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Module 5 Flashcards

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1
Q

Why phosphorylate?

A
  1. Changes the glucose molecule so it is unable to leave the cell through glucose transporters in the cell membrane.
  2. Maintains the glucose concentration gradient for diffusion of glucose out of the blood and into the cell, as it doesnt affect the glucose concentration
  3. Takes the glucose to a higher energy level. This makes it unstable and therefore more reactive, so it is easier to split.
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2
Q

Why is the mitochondria the location of respiration?

A

cristae have large SA for oxidative phosphorylation

matrix as has enzymes needed for krebs cycle and link reaction

outer mitochondrial membrane seperates contents from rest of cell and creates cellular compartment for conditions ideal for aerobic respiration

inner mitochondrial membrane contains electron transport chains and ATP synthase

intermembrane space has protons pumped into it. small space so concentration builds up quickly

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3
Q

Anabolic

Catabolic

A
  • Building larger molecules from smaller molecules (using energy – endergonic).
  • Breakdown of larger molecules to smaller molecules (releasing energy – exergonic).
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4
Q

Metabolic pathway

Metabolites/ intermediates

Metabolism

A
  • A sequence of metabolic reactions.
  • The individual molecules in the pathway.
  • The net result of anabolism and catabolism.
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5
Q

Glycolosis

A

Occurs in cytoplasm of all cells where glucose is broken down into pyruvate. Does NOT need oxygen.

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6
Q

Link reaction

A

Occurs in matrix of mitochondria. Pyruvate is dehydrogenated (hydrogen removed) and decarboxylated (carboxyl removed) and converted to acetate.

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7
Q

Krebs cycle

A

Occurs in the matrix of mitochondria. Acetate is decarboxylated and dehydrogenated.

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8
Q

Oxidative phosphorylation

A

Occurs on the folded inner membrane (cristae) of mitochondria. This is where ADP is phosphorylated to ATP.

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9
Q

What is CoA made of and what is its function?

A
  • Made from pantothenic acid (B-group vitamin), adenosine (ribose + adenine), 3 phosphate groups and cysteine.
  • CoA carries the acetate (ethanoate) groups made in the link reaction into the Krebs Cycle.

image

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10
Q

What is NAD?

What is is made of?

What does it do?

A
  • Organic, non-protein coenzyme called nicotinamide adenine dinucleotide (NAD)
  • Made of 2 linked nucleotides.
  • Made in the body from nicotinamide (Vitamin B3), 2 ribose, adenine and 2 phosphate groups.
  • It is the nicotinamide ring that can accept hydrogen atoms.
  • When NAD accepts two hydrogen atoms it is known as reduced NAD.
  • The reduced NAD transports the hydrogen to the inner mitochondrial membrane, where it will be used to generate more ATP in the electron transport chain.
  • Once it has dropped off the hydrogen in the mitochondrion the NAD is in its oxidised form again and free to accept more hydrogen
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11
Q

Why does reduced NAD and FAD actually contribute less ATP?

A
  • Some of the ATP produced is used to actively transport pyruvate from the cytoplasm of the cell into the matrix of the mitochondrion.
  • Some ATP is used to bring reduced NAD from glycolysis in the cytoplasm into the mitochondrion.
  • Some energy is used to transport ADP from the cytoplasm into the mitochondrion.
  • Some H+ ions leak back across the mitochondrial membrane reducing the proton motive force that generates ATP.
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12
Q

Electron transport chain stages

A
  1. Reduced NAD delivers 2 hydrogen atoms to Complex I. These atoms split into 2H+ ions and 2e-. The electrons are passed on to Complex II and this process releases enough energy to pump the H+ ions against their concentration gradient from the matrix into the intermembrane space of the mitochondrion.
  2. The electrons from NAD continue from Complex II to Complex III. The energy released at this stage is NOT enough to pump H+ ions from the matrix into the intermembrane space.
  3. Reduced FAD from the Krebs Cycle drops off 2H atoms directly to Complex II (bypassing Complex I). Again, these hydrogen atoms split into 2H+ and 2e-. The electrons are passed onto Complex III but the H+ ions remain in the matrix due to lack of energy for pumping at this stage.
  4. The four electrons (the 2 from the NAD and the 2 from the FAD) pass from Complex III to Complex IV. The energy released is enough to pump H+ions from the matrix into the intermembrane space.
  5. The 4 electrons move from Complex IV into the matrix where they combine with 4H+ ions and O2 to form H20. The energy released at this stage IS enough to pump H+ ions into the intermembrane space.
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13
Q

Chemiosmosis

A
  • The pumping of H+ ions into the intermembrane space generates a electrochemical gradient and a proton (pH) gradient. This generates a proton motive force that should lead to the diffusion of H+ ions back into the matrix.
  • However, the membrane is relatively impermeable to H+ ions, and the only way they can return to the matrix is through the ATPsynthase enzyme complex.
  • As the H+ moves through this complex it catalyses the formation of ATP from ADP and Pi.
  • It is this stage that is known as oxidative phosphorylation. You are phosphorylating the ADP to form ATP by using oxygen as the final electron acceptor (gets reduced) of the electron transport chain to form water
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14
Q

Respiratory substrates definition

A
  • A respiratory substrate is an organic molecule that may be used in respiration to release energy.
  • Different substrates release different amounts of energy when respired.
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15
Q

Glucose as a repsiratory substrate

A
  • Glucose is the main respiratory substrate (the brain can only use glucose).
  • starch and glycogen can be broken down into glucose and other carbs can be changed to glucose by isomerisation
  • carbs release 16 energy KJ g-1
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16
Q

Protein as a respiratory substrate

A
  • When starving, protein can also be used.
  • Protein is hydrolysed to amino acids.
  • It can be converted to pyruvate, acetate or enter the Krebs cycle directly.
  • 17 KJg-1 energy
  • There is a little more energy released as the number of hydrogen atoms accepted by NAD per aa is slightly more than for a molecule of glucose
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17
Q

Lipids as respiratory substrates

A
  • Lipids are an important respiratory substrate (especially for muscles).
  • They are first hydrolysed to glycerol and fatty acids.
  • Glycerol can be converted to glucose and join the glycolysis pathway.
  • Fatty acids combine with Acetyl Co-A used in krebs cycle. This is called the beta oxidation pathway which produces reduced NAD and reduced FAD
  • 39 KJg-1 energy
  • lots of ATP as lots of H atoms, so lots of reduced NAD and greater proton motive force/gradient. most ATP comes from oxidative phosphorylation in repsiration
  • Also use more oxygen to respire as produce more water
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18
Q

How much energy is needed to produce 1 molecule of ATP?

A

30.6KJ

lots of energy is lost as heat instead of producing ATP

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19
Q

What is the equation for respiratory quotients?

How do you get the values?

what are the values for carbohydrates, lipids and proteins?

A

Co2 released/ 02 uptake

using a respirometer

carbs: 1 (6CO2 molecules required to completely repire 1 molecule of glucose producing 6CO2)
proteins: 0.9
lipids: 0.7

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20
Q

What values do aerobic, anaerobic and combination respiration produce?

A

normally 0.8-9 showing a mixture of respiratory substrates used

a combination of anaerobic and aerobic produces a RQ greater than 1 but its hard to tell when anaerobic starts

purely anaerobic has a infinity

only aerobic is less than 1

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21
Q

Explain the method for the respirometer (measures volume of oxygen used in living organisms)

A

1. carefully weigh out 5g of soda lime pellets (absorb co2 so o2 taken up can decrease the volume and cause dye to be drawn up equivalent to volume of O2 used) and add to tube A and B

  1. fill the wire basket for tube A with 5g of maggots and place into tube A, being careful the maggots dont touch the soda lime pellets as they are very corrosive
  2. fill the wire basket for tube B with 5g glass beads and place into tube B. This is as a control with the same mass/vol as the maggots so that any external factors affecting 1 side will affect the other the same without respiring. dead maggots would be better. increase in temperature would would increase gas volume but will happen in both tubes no overall effect- valid measurements
  3. the repirometer U-tube has already been filled with manometer fluid. connect the respirometer to the two tubes making sure the 3 way taps are both turned to the upward position so the equiptment is open to the atmosphere while setting up the experiment
  4. turn both taps to the downward position and note the position of the manometer fluid and start the timer
  5. after 10 minutes record the distance the manometer fluid has moved. use formula to see how many cm3 1 division is
  6. calculate volume of oxygen comsumed in min-1g-1 for the maggots- pier2

beaker of water can control temperature but not all equiptment in water

syringe for repeats

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22
Q

What happens to the lactate formed in anaerobic respiration?

A
  • carried away in the blood to the liver
  • when more oxygen is avaliable the lactate is converted back to pyruvate to enter the kerbs cycle or its recycled back into glucose and glycogen
  • muscle fatigue is not caused by a build up of lactic acid but actually the reduction in pH from lactate dissociating into lactic acid that reduces enzyme activity in the muscle cells
  • reduces amount of ATP cannot mainatin vital processes for a long period of time, as only 2 ATP from glycolysis
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23
Q

Facultative anaerobe

Obligate anaerobes

Obligate aerobes

A
  • can live without oxygen, but uses it when is present eg. yeast
  • cant survive in the presence of oxygen
  • need oxygen eg mammals as O2 is eventually required and products of anaerobic need to be broken down by O2
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24
Q

Why can anaerobic respiration occur in yeast?

How is yeast grown for alcohol?

A

The enzyme pyruvate decarboxylase is only in yeast

Yeast grows faster in aerobic conditions so in the brewing industry the yeast is first grown with oxygen then grown under anaerobic conditions for alcoholic fermentation to take place

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25
Q

How does the lack of oxygen cause anaerobic repsiration and how does anaerobic respiration allow us to continue respiring?

A
  • No O2 to act as final electron acceptor at the end of the electron transport chain in oxidative phosphorylation so flow of electrons stops and synthesis of ATP by chemiosmosis stops
  • As no flow of electrons, reduced FAD and NAD can no longer be oxidised as there is nowhere for electrons to go so NAD and FAD cant be regenerated so so the decarboxylation and oxidation of pyruvate and kerbs cycle comes to a halt
  • fermentation allows glycolysis to continue by providing NAD in glycolysis
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26
Q

Be familiar with the names of these proteins in the electron transport chain

A

Complex 1: NADH Coenzyme Q (oxidoreductase)

Complex 2: succinate coenzyme Q (oxidoreductase)

Complex 3: Coenzyme Q Cytochrome C (Oxidoreductase)

Complex 4: Cytochrome C (oxidase)

Complex 5: ATP synthase

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27
Q

Investigating dehydrogenase activity in anaerobic and aerobic respiration of yeast

A

A- yeast

B-yeast (boil after to check boiling isnt affecting colour)

C- dead yeast (boiled)

D- yeast with layer of oil to make anaerobic

Method:

  1. 10cm3 of yeast in alll tubes
  2. boil C using bunsen burner and large beaker for 5 mins then cool under cold running tap
  3. add 1cm3 of methylene blue to each tube and oil to D
  4. rubber bung on each tube and gentyl shake to mix to uniform colour
  5. put other tubes in 40oC water bath and check using thermometer for 10 mins. make observations
  6. boil B then allow to cool
  7. shake tube A vigourously and note observations. this adds o2 so reoxidises methylene blue
  8. shake tube B and note observations

methylene blue acts as NAD, taking H and being reduced (arificial hydrogen acceptor)

enzyme controlled as affected by temperature

methylene blue is reduces to colourless and reoxidised to blue

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28
Q

Homeostasis definition

A

maintaining conditions constant within a normal range despite external factors changing

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29
Q

What is the external environment?

A

the air, soil or water around an organism

any changes must be monitored and respond (behavioral or physiological) to in order to reduce stress

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30
Q

The internal environment

A
  • conditions inside the body
  • the environemnt influencying cells is tissue fluid
  • it may change due to products of metabolism diffusing into tissue fluid EG. CO2 waste product of respirtaion can change pH of environment and enzyme action
  • blood helps maintain internal environment by removing wastes or toxins, preventing them accumulating in the tissue fluid.
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31
Q

Why are communication systems needed?

Features of a good communication system?

A

Multicellular systems need to pas info between their parts to coordinate responses

  1. specific target cells complementry
  2. goes throughout body
  3. short and long term
  4. fast
  5. allows intercellular communication
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32
Q

Cell signalling

A
  • the process by which information is passed from 1 cell to another
  • 1 cell releases a chemical that is detected by another cell. the 2nd cell responds
  • there a 2 main cell signalling systems:
  1. nueronal (network of neurones that signal across synapses. Rapid short term changes)
  2. hormonal (blood transports signals recognised by specific TT. Slower and long term effects)
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33
Q

Stimulus response pathway

A
  1. stimulus
  2. detected by a receptor
  3. processed by a communication system
  4. effector
  5. gives a response
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34
Q

Receptors-

Effectors-

A

monitor conditions inside the body. if a change is detected, the recpetor is stimulated to communicate with the effector

cells whcih respond to the reverse change (gland or muscle)

  • information from sensory receptors is transmitred to brain and impulses sent along motor neurones to effectors to bring about changes to restore equilibrium
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35
Q

Negative feedback

A

process that results in a reversal of amny change in internal conditions away form a steady state. it ensures optimum internal conditions are maintained and is essential for homeostasis

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36
Q

positive feedback

A

the process that increases any change detected by the receptors. it is less common and doesnt help homeostasis

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37
Q

Positive feedback examples

A
  1. blood clotting cascade- platelets stick to damaged region and release clotting factors, innitiating clotting and attracting more platelets and enhances effect until clot forms
  2. childbirth- head presses against cervix stimulating production of oxytocin hormone. this stimulates uterus to contract, pushing head of baby harder against verxix and triggering more oxytocin. this continues until the baby is born (outside factor brings it to an end)
  3. hypothermia- low metabolic activity from old age and not moving much. this means little heat is produced and the cold means enzyme ROR slows. this means even less heat is produced so ROR slows more.
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38
Q

what are ectotherms?

How do ectotherms control their temperature?

A

cold blooded

behavioural responses to warm

  • bask in sun eg lizards
  • orientate body so large SA exposed to sun eg. butterfly
  • extend areas of body to be exposed by sun
  • conduction by pressing body to warm ground

behavioural responses to cool

  • prevent enzyme denaturing by shading in rocks
  • dig burrows
  • press against cool earth
  • water (is stable due to high specific heat capacity so little thermoregulation needed)
  • light colour
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39
Q

What are features of ectotherms?

why is it important to be warm?

A
  1. can tolerate a wider temperature range
  2. have restricted behaviour
  3. can last longer without food as have lower metabolic rate

can move fast, catch prey, escape predators

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40
Q

Ectotherm

A

animal that obtains most its heat from outside their body so their temperature fluctuates with the environment. they cant increase respiration rate to generate heat

eg fish, reptiles, amphibians

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41
Q

endotherms

How do they loose heat?

A

organisms that can genrate heat with their bodies (exergonic reactions- release energy) to maintain body temperature

eg mammals and birds

5x faster metabolic rate than ectotherms so need more food

can loose heat by:

  • evapouration of water
  • conduction and convection
  • radiation (reduced by clothes that trap air)

Can gain heat by:

  • waste from cell respiration
  • conduction from surroundings
  • convection from surroundings
  • radiation from surroundings
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42
Q

Graph of body temperature vs environmental temperature

what is human core body temperature?

A

endotherms can maintain temperature independent of the environemental temperature

ectotherms are more dependent on the environmental temperature

36.8- above enzymes denature and below metabolism slows down

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43
Q

How does the body control core body temperature?

what are the temperatures indicating fever and hypothermia?

A

thermoreceptors in the thermoregulatory centre of the hypothalamus detects changes in core body temperature

it also recieves nerve impulses from the peripheral thermoreceptors in the skin of the extremities

35 and 38

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44
Q

What physiological changes correct overheating?

A
  1. vasodilation- arterioles dilate, smooth muscle relaxes and diameter of lumen increases. increased volume of blood and blood flow to capillaries at surface- radiation. pre capillary sphincters also close
  2. sweating- weat glands secrete a dilute solution of mostly water, but also sodium chloride and urea. Evapouration of water leads to loss of heat by the body as waters high latent heat of vapourisation means heat is absorbed from the skin as water evapourates.
  3. flattening of hairs- errector muscles at base of hair relax so hairs lie flat and air doesnt form an insulating layer
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45
Q

What physiological changes correct overcooling?

A
  1. vasoconstriction- of arterioles near skin surface. little radiation as blood is diverted through shunt vessels (ateriovenus shunt vessels dilate) deeper in skin reducing the cooling effect
  2. decreased sweating
  3. errecting hairs- muscle contracts, pulling the hair up and traps a layer of warm, still air around the hair to insulate the organism and retain heat
  4. shivering- nervous reflex, rapid, involuntary regular muscle contraction generates heat by metabolic reaction, as more ATP needed so more respiration in muscle and warms blood from heat biproduct
  5. thyroxine released from thyroid gland to boost basal metabolic rate and heat production

the cerebellum of the human brain makes people feel hot or cold so they adapt their behaviour appropriately

effectors are- skin arteroiles, skeletal muscle, sweat glands

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46
Q

What hormones are produced in these glands?

  1. testes
  2. adrenal
  3. ovaries
  4. thyroid
  5. pancreas
  6. anterior pituitary
  7. posterior pituitary
A
  1. testosterone
  2. cortisol, adrenaline
  3. progesterone, eostrogen
  4. thyroxine
  5. insulin, glucagon
  6. growth hormone, LH, FSH
  7. oxytocin, ADH
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47
Q

Endocrine system definition

A

chemical messenger sysem made of glands and organs that make hormones and secrete them into blood so they can transport to TT

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48
Q

Hormone definition

A

chemical messenger transported in the blood, secreted by endocrine glands to receptors on cells in target tissue plama membrane, have an effect on one or more target tissues

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49
Q

Endocrine gland definition-

exocrine gland defintion-

A

a group of cells specialised to secrete chemical hormones directly into blood as ductless

secretes other substances through a duct not into the blood

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50
Q

Target tissue definition-

A

specific complementry receptors for a hormone

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51
Q

Secretion definition

A

process by which substances are produced from a cell, gland or organ for a particular function or excretion

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52
Q

Protein hormones method of action

example and its gland, cause, TT

A
  • not soluble in cell membrane so dont enter the cell
  • have to have a secondary messenger by binding to specific receptors on plasma membrane or target cells, triggering a cascade reaction

EG. adrenaline

is secreted by the adrenal glands in response to stress

target tissues include the SA node, smooth muscle in the gut wall, iris muscles in the eye, liver

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53
Q

Steroid hormones

A

can pass through the phospholipid bilayer and directly effect the DNA in the nuclues using lipid soluble cytoplasmic receptors

EG. oestrogen

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54
Q

Adrenaline cascade

A
  • Adrenaline (first messenger) binds to receptor in cell membrane of TT
  • this alters the receptors shape, causing a G protein molecule attached to receptor to split
  • part of the G protein then binds with the enzyme adenyl cyclase, activating it
  • adenyl cyclase converts ATP to cAMP (second messenger) which can activate other enzymes inside the cell
  • glycogen converted to glucose
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55
Q

Adrenal gland structure

A

sit above kidney

cortex with medulla in the middle

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56
Q

Function of adrenal cortex

A
  1. Production of hormones is controlled by hormones released from pituitary gland in brain, mainly steroid hormones
  2. Releases Glucocorticoids hormones like cortisol which help regulate the metabolism, by controlling how the body converts fats, proteins and carbs to energy. Also regulates blood pressure and how the cardiovascular system responds to stress. Corticosterone regulates the immune response. The hypothalamus controls the release of these hormones.
  3. Mineralocorticoids like aldosterone control blood pressure by maintaining salt and water concentrations. The kidney triggers signals which control the release.
  4. Androgens are small amounts of male and female sex hormones that can be important in women after menopause.
  5. Produces hormone essential for life
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57
Q

Function of adrenal medulla

A
  1. Hormones released when the sympathetic nervous system is stimulated, when the body is stressed.
  2. Adrenaline is released which increases HR, sending blood quickly to the muscles and brain, as well as increasing blood glucose by hydrolysing glycogen to glucose in the liver.
  3. Noradrenaline is a hormone that also works in response to stress. It increases HR, widens pupils, widens air passages in lungs, narrows blood vessels in non essential organs (creates higher BP)
  4. Produces non-essential for life
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58
Q

Glucose cotransport

A

symport cotransporter

allows facilitated diffusion of glucose into a cell

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59
Q

Insulin secretion

A

beta cell

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60
Q

What is diabetes mellitus

Types of diabetes:

  • when do you get it
  • what is it
  • why do you get it
  • treatment

Symptoms

A

A condition where the body cant maintain steady state blood glucose concentrations leading to hyperglycaemia after a meal or hypoglycaemia after exercise or fasting

Type 1:

  • starts in childhood
  • not enough insulin is secreted so excess glucose isnt stored as glycogen
  • possibly due to autoimmune attack on B cells, virus or genetic link
  • regular injections of insulin, test blood regularly by pricking finger, insulin increases amount of glucose taken up by cells cauing glycogenesis

Type 2:

  • produce insulin but as they age their body response decreases
  • possibly due to decline in receptors and amount of insulin secreted
  • induced earlier by obesity
  • regulate carb intake through diet to match exercise
  • drugs can be used to stimulate insulin production or slow rate body absorbs glucose from intestine
  • insulin injections
  • thirsty, hungry (cant absorb glucose for respiration and energy)
  • pee more than usual
  • tired
  • loose weight
  • blurred vision
  • hyperglycaemia
  • glucose in urine (excessive conc. of glucose in blood so kidneys cant reabsorb it all)
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61
Q

Current and future treatment for diabetes

A
  • insulin obtained from pancreas of cows and pigs slaughtered for food.
  • this can be difficult and expensive
  • can cause allergic reactions as they are a bit different to human
  • pancreas transplant
  • long waiting list
  • can be risky and need immunosuppresent drugs
  • now made by genetically modified bacteria
  • less likely allergic reactions
  • can be produced in higher quantities
  • cheaper to produce
  • religious/ ethical issues using animal products is overcome
  • research into totipotent stem cells and the signals required to promote differentiaition into B cells, either in patient or before transplanted. likely stem cells will be taken from embryos spare from fertility treatment/ terminated pregnancy. can also use preserved umbillical stem cells.
  • the embryo is destroyed but often destroyed anyway
  • 1 embryo does many treatments
  • donor available not an issue as unlimited new B cells
  • reduced likelyhood of rejection
  • people dont have to inject themselves with insulin
  • limited knowledge so may form tumours due to unlimted cell growth
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62
Q

Structure of the pancreas

A
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63
Q

exocrine role of the pancreas

A

Acinar

  • Small groups of cells around a tubule secrete pancreatic juice.
  • The tubules join to form the pancreatic duct which empties the fluid into top part of the small intestine- duodenum
  • Juice contains enzymes such as lipases, amylase and trypsin
  • Juice contains sodium hydrogen carbonate to neutralise the stomach acid
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64
Q

Endocrine role of the pancreas

A
  • Regulation of blood glucose (normally 80 -120mg/100ml blood)
  • Glucose is stored in the liver and muscle cells as glycogen
  • Changes in blood glucose are detected by receptors which are cells of the Islets of Langerhans
  • Produces hormones and releases them into blood- beta cells secrete insulin and alpha cells (larger and less numerous) secrete glucagon
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65
Q

Why is it important to regulate blood glucose levels?

A
  • all cells need glucose as a respiratory substrate
  • brain cells only use glucose for respiration so its critical to maintain constant levels
  • changes in blood glucose often affects osmotic potential of blood
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66
Q

Histology of the pancreas

A

islets of langerhans are circular light areas

solid white circle may be branch of the pancreatic duct or vein

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67
Q

What happens when there is an increase in blood concentration?

A
  1. Rise in blood glucose concentration
  2. detected by beta cells in islets of langerhans in pancreas
  3. repsonse is for beta cells to secrete insulin directly into blood as ductless
  4. insulin is transported to target tissues and binds to receptors to activate adenyl cyclase.
  5. converts ATP to cAMP activating a cascade of reactions
  6. increase cellular uptake of glucose in liver and muscle and converts it to glycogen (glycogenesis) through change in tertiary structure of glucose transport protein channels so they open.
  7. respiration increases
  8. glucose also converted to lipids
  9. inhibits the release of glucagon from alpha cells
  10. glucose concentration falls
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68
Q

What happens when there is a fall in glucose concentration?

A
  1. detected by alpha cells in iselts of langerhans in pancreas
  2. response is for alpha cells to secrete glucagon directly into blood as ductless
  3. glucagon transported to TT and binds ot receptors on liver and fat cells to innitiate a second mesenger
  4. glycogenolysis- glycogen stored in lover and muscle cells broken down into glucose and released into blood stream (hydrolysed)
  5. Gluconeogenesis- production of glucose from non carb sources like glycerol and aa
  6. less glucose absorbed
  7. eating- absorbtion of products of carb digestion
  8. increased levels of blood glucose
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69
Q

Secretion definition

Egestion definition

Excretion definition

A

the production of a sunstance from a gland

the expulsion of undigested food from the body

the removal of metabolic waste from the body which if permitted to accumulate would become toxic and prevent maintenance of a steady stae eg CO2 from aerobic respiration and urea from protein metabolism

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70
Q

Why do we excrete?

A
  1. to prevent the unbalancing chemical equilibria
  2. to prevent waste products affecting metabolic activity by acting as an inhibitor or toxin
  3. to regulate ionic content of body fluids
  4. to regulate water content of body fluids tp regulate H+ and hence pH of body fluids
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71
Q

Waste products

A

CO2 (lungs)- from aerobic respiration in mitochondria. would lower pH, damaging cells

Ammonia- deamination in liver cells. increases pH in cytoplasm affecting metabolic processes and receptors for neurotransmitters

Urea (kidneys, skin)- ornithine cycle. diffuses into cells and decreases water potential so cells absorb water and burst

bile pigments (small intestine)- breakdown of haem group in liver so accumulate in skin. jaundice

Uric acid- breakdown of purines. can form crystals in joints causing gout.

water (skin, lungs, kidneys)

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72
Q

Removal of nitrogenous compounds

A
  • Excess protein in the diet cannot be stored.
  • AA contain almost as much energy as carbs.
  • AA transported to liver and the amino group is removed – deamination and the keto acid can be used in respiration
  • The amino group dissolves to form toxic ammonia which is detoxified to urea and transported in the plasma to the kidney for excretion.
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73
Q

Excretion of CO2

Respiratory acidosis

A
  1. dissolved in plasma
  2. carbonic acid and hydrogen carbonate ions (has enzyme so faster in RBC)
  3. carbamino haemoglobin

•CO2 dissolves in blood plasma forming carbonic acid.

CO2 + H2O H2CO3

•Carbonic acid dissociates to release H+ ions

H2CO3 H+ + HCO3-

  • H+ ions make the blood more acidic. A small change is detected by the medulla oblongata, which results in an increase in breathing rate to remove excess CO2.
  • A large change can cause symptoms of acidosis – slowed breathing, headache, drowsiness, restlessness, tremor and confusion as well as changes in blood pressure and rapid heart rate.
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74
Q

Where is the liver located?

Facts about the liver

A
  • top right portion of the abdominal cavity just under the diaphragm
  • largest organ containing 13% of total blood volume at a time, acting as a resevoir to compensate for small changes in blood volume
  • uses up 20% of bodys energy
  • composed of left and right lobes enclosed by fibrous Glissons capsule
  • each lobe is formed of hexagonal lobules
  • recieves blood from 2 vessels- hepatic artery and portal vein (brings blood from intestines to liver along with products of digestion
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75
Q

Hepatocytes

How to recognise triad

A
  • Make roughly 80% of the mass of the liver
  • nuclei are distincly round
  • hepatocytes are exceptionally active in synthesis of protein and lipids for export so have large amounts of SER and RER and golgi and mitochondria
  • lots of glycogen granules and vesicles containing very low density lipoproteins

Kupffer cells help digest products which need removing by phagocytosis. the liver breaks down old red blood cells

  1. branch of hepatic portal vein largest
  2. artery is more muscular walls and smaller lumen
  3. bile duct is left over
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76
Q

Sinusoids

what do hepatocyes absorb and release?

Phagocytic cells

A
  • in between cords of hepatocytes, there are channels filled with blood called sinusoids.
  • the blood passes from the hepatic artery and hepatic portal vein into the sinusoid and flows between the hepatocytes to enter the hepatic vein in the centre, where rapid exchange can occur.
  • sinusoids are lined with incomplete layer of endothelial cells allowing the blood to reach hepatocytes
  • hepatocyes lining the sinusoids have microvilli to increase SA

Hepatocytes

–Release: plasma proteins (prothrombin, albumin, fibrinogen), lipoproteins and cholesterol

–Absorb: insulin, glucose, minerals, vitamins, blood borne toxins for detox.

Kupffer cells in sinusoid help digest products which need removing by phagocytosis. ingest bacteria from blood and breakdown bilirubin for absorption into hepatocytes

  • hepatic cells lining the canaliculus make and secrete bile
  • this flows from the middle to the outside and enters branch of the bile duct.
  • doesnt connect to hepatic vein
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77
Q

Bile canaliculus

functions of bile

A
  • hepatic cells lining the canaliculus make and secrete bile
  • this flows from the middle to the outside and enters branch of the bile duct which delivers bile into the duodenum, diverting through the gall bladder (bile stored here).
  • doesnt connect to hepatic vein
  • Hepatocytes close to a bile canaliculus are rich in Golgi apparatus for transport of bile constituents into the channels
  1. emulsifies fats- increases SA for lipase so faster metabolism
  2. antibacterial
  3. neutralise stomach acid
  4. important for absorption of fat soluble vitamins from digested food
78
Q

Colour of bile

composition of bile

what makes bile

disease

A
  • Bile is a yellowish-green liquid that hepatic cells secrete
  • It includes water, bile salts, bile pigments, cholesterol, and electrolytes.
  • Bile salts are made from cholesterol and emulsify fats to aid lipase in digestion.
  • Bile pigments are breakdown products from red blood cells (bilirubin and biliverdin)
  • If the liver can not excrete the bilirubin quickly enough it builds up under the skin causing jaundice
79
Q

Functions of the liver

A
  1. immune system- Macrophages called Kupfer cells
  2. detoxification of- Alcohol, Drugs, Ammonia, aa
  3. Control levels of- Lipid (storage in adipose), Glucose, Amino acids
  4. Stores- Glucose as glycogen, Minerals Cu and Fe, Key Vitamins A, D, E, K and B12, Saturated fat
  5. Removal of- Bilirubin (haem group from old RBC, Used hormones e.g. sex hormones
  6. Synthesis and secretion- Plasma proteins (inc clotting factors), Red blood cells (in foetus), Bile, Glucose, Cholesterol and lipoproteins, Heat
80
Q

Formation fo urea

A

Excess aa in the diet cant be stored as the amine group makes them toxic so the urea is deaminated forming a keto acid and ammonia (toxic)

the keto acid can enter respiration directly to release energy (gluconeogenesis)

the ammonia enters the ornithine cycle to form less toxic, soluble urea for excretion by the kidneys

81
Q

Ornithine cycle

A

ammonia combines with CO2 to produce urea

urea is reabsorbed back into the blood and is transported back to the kidneys where its filtered into the urine

urine is stored in the bladder until it is released from the body by excretion

2NH3 + CO2 –> CO(NH2)2 + H2O

Urea: (NH2)2-C=O

82
Q

Detoxification

A
  • Toxins may be produced by our body (e.g. hydrogen peroxide), may be taken in via our diet (e.g. alcohol), or may be consumed recreationally/medicinally (e.g. drugs).
  • Toxins can be oxidised, reduced, methylated or combined with another molecule to make them harmless.
  • Liver cells contain many enzymes that make toxins less toxic e.g. catalase breaks down hydrogen peroxide into oxygen and water
83
Q

Detoxification of alcohol

A
  • Ethanol (alcohol) depresses nerve activity.
  • It contains energy so can be respired.
  • It is broken down by hepatocytes to ethanal by the enzyme ethanol dehydrogenase.
  • Ethanal dehydrogenase then breaks the ethanal down into ethanoic acid.
  • Ethanoic acid combines with coenzyme A to form acetyl coenzyme A which can enter the respiratory pathway.
  • The H+ions released during this process are used to reduce the coenzyme NAD to form reduced NAD.
  • NAD is also used in respiration to break down fatty acids.
  • If the liver has to detoxify too much alcohol it has insufficient NAD to deal with the fatty acids (used in metabolims of ethanol) and so these are converted back to lipids to be stored in the liver. This leads to the “fatty liver” condition and can lead to hepatitis or cirrhosis.

Ethanol (-> NAD then reduced NAD) –> ethanal (->NAD then reduced NAD) –> ethanoc acid –> acteyl coenzyme A–> to respiration

84
Q

Structure of the kidney

A

Capsule- thin layer of connective tissue with collagen fibres for protection

cortex- dark outer layer where filtering of blood occurs and dense capillary network form renal artery to nephrons. ultrafiltration and selective reabsorption

medualla- lighter, tubes of nephrons form pyramids

pelvis- central chamber where urine collects before passing down the ureter

ureter- thick walled muscular tube moves urine to bladder by peristalsis

85
Q

A3 sheet for nephron processes

A
86
Q

microscope diagrams on paper

A
87
Q

Glomerular filtration rate

A
  • rate at which blood is filtered in the kidney by ultrafiltration
  • can indicate kidney disease if below 60 and kidney failure if less than 15cm3/min
  • lower the rate, the less efficient the kidney
  • a substance like inulin can be injected into blood stream and its removal rate measures. passses into urine and not reabsorbed
  • can also measure removal rate of wastes like creatinine (breakdown product of muscle) if high, kidneys arent working
88
Q

Adaptations of the PCT for reabsorption

A
  1. miccrvilli on lumenal side- SA for reabsorption and many symport carriers
  2. cuboidal epithelium- pack tightly together
  3. 1 cell thick tubule- short diffusion distance
  4. mitochondria- produces ATP for active transport
  5. proximity of peritubular capillaries- short diffusion distance, maintains diffusion
  6. folded membrane on capillary side- SA for rebsorption and protein pumps
  7. co-transport proteins- allows facillitated diffusion
  8. protein pumps- active transport of proteins for sodium and potassium
  9. RER- makes proteins for pumps, symport carrier proteins
  10. tight junctions- prevent substances slipping through
89
Q

Symptoms of kidney failure

A

oedema- swelling due to accumulation of fluid in tissues

dehydrated

urine may contain blood, protein and be cloudy

anaemia and tiredness- as kidneys stop producing erythropoetin

rashes, nausea- due to build up of toxins

90
Q

Causes of kindey failure

A

usually due to inflammation of glomeruli

common in older people and diabetics

acute failure can be reversed but chronic may need renal dialysis treatment

Acute:

  1. infection where podocytes and tubules are damaged
  2. loss of large amount of blood or tissue fluid
  3. blockage preventing drainage of urine from kidney eg kidney stone

Chronic:

  1. compliction fo diabetes
  2. raised BP can damage structure of epithelial cells and basement membrane
  3. infammation of kidney tissue
  4. genetic conditions like polycystic kidney disease (fluid filled cycsts)
91
Q

Diagnosing kidney disease

A
  1. symptoms like cloudy or bloody urine
  2. ultrasound and CT look for blcokages
  3. analyse urine samples for blood cells and protein as these are too big to pass through basement membrane.
  4. analse blood samples, as waste substace creatinine increases as kidney disease progresses as failing kidneys dont remove wastes from blood
92
Q

Effects of kidney disease

A
  1. toxic urea can build up in blood poisoning cells
  2. hgih BP as kidneys control it my maintaining water balance.
  3. abnormal proteins building up in blood creates painful and stiff joints
  4. anaemia- kidneys produce hormone erythropoietin which stimulates formation of RBC. less RBC produced results in tiredness
  5. build up of K+ ions associated with abnormal cramps, tiredness, affects impulses from SANand lead to arythmia and cardiac arrest
93
Q

Why must the salt intake of a person with kidney failure be carefully controlled?

A

sodium chloride builds up in blood altering water pot. of blood plasma leading to retention of water, excessive thirst and cardiac arrest

94
Q

treatments of kidney failure (haemodialysis)

A

Haemodialysis

  • This removes waste products from the blood by passing it out of the body, through a filtering system (dialyser) and returning it, cleaned, to the body through vein.
  • Hard to access arteries so can create arteriole loop
  • heparin is added to blood to prevent blood clotting in dialysis machine
  • Blood leaves the artery and passes between layers of a partially permeable membrane mimics basement membrane of bowmans capsule (not proteins tho) that allows the waste products (which are much smaller than blood cells) to pass out through it. flows counter current to dialysate to miantain steep conc. gradients
  • The membrane is bathed in isotonic fluid with normal ions, glucose and water potential. this ensures useful substances arent removed, only if in excess. no urea in dialysate so all removed
  • Anything in xs in the blood crosses the membrane into the dialysis fluid
  • A patient will need haemodialysis for about 5 hrs 4 times a week. the temperature is the same as the blood due to enzymes and so the person doesnt get dehydration or overhyration by feeling warm or cold
95
Q

treatments of kidney failure (peritoneal dialysis)

advantages and disadvantages

A
  • Dialysis fluid is placed around the membrane lining the intestine (peritoneal membrane) and toxins and excess water diffuse out of the blood and into the tissue fluid, across peritoneal membrane into dialysis fluid, which is regularly changed 2 or 3 times a day
  • fluid goes in and out through a catheter
  • The patient remains mobile and does not have to go to hospital for this treatment.
  • Is a continuous process so avoids swings in blood composition
  • readily available
  • High risk of infection
  • Has to be carried out regularly
  • have to monitor diet, cant ingest too much salt
  • expensive long term
  • eventually causes damage to body
96
Q

treatment of kidney failure (transplant)

advantages and disadvantages

A

single kidney

dont remove kidneys

blood vessels joined and ureter inserted into bladder

  • lasts many years if successful
  • immunosuppresents lifelong so risk of infection
  • risk of surgery
  • lack of donors as need to be healthy. less road accidents, stroke, heart attack
  • black market trade illegally
  • try to match antigens but can reject
  • last 9-10 yrs then return to dialysis
97
Q

the future for kidney disease

A
  1. could explore xenotransplantation where kidneys fro other organisms used (pigs)
  2. stem cells to grow a kindey- 2011 grew functioning embryonic kidney tissue from stem cells. in future could grow a whole one with no antigens that trigger immune response so now drugs needed
98
Q

what does a longer loop of henle mean?

A

longer loop of henle conserves more water as can do moe active trabsport as more sodium carrier proteins so lower water pot. in medulla so more water is reabsorbed at the collecting duct

99
Q

osmoregulation

how is water gained and lost

A

the control of water levels and salts in the body, vital for homeostasis. works by negative feedback

water is gained from food, drink, metabolism

water is lost from urine, sweat, exhaled water vapour, faeces

100
Q

diabetes insipidus

A

when you dont release enough ADH so large urine volumes and dehydration

101
Q

How are monoclnal antibodies made for a pregnancy test?

A
  • monoclonal antibodies are antibodies from a single clone of cells that are produced totarget particular cells/chemicals
  • mouse is injected with HCG (produced from developing placenta and prevents period and maintains pregnancy until placenta takes over) so it makes the appropriate antibody
  • the B cells that make the required antibody are removed from the mouse spleen and fused with a myeloma (type fo fast dividng cancer cell)
  • its now known as a hybridoma which reproducs rapidly making lots of cells and making lots of antibodies
  • monoclonal antibodies are colected, purified and used
102
Q

How does a pregnancy test work?

A
  • Pregnancy testing kits test for HCG in urine
  • Monoclonal antibodies to HCG coat a dipstick
  • The antibodies may be bound to gold
  • The stick is dipped in urine, the HCG in the urine binds to the monoclonal Ab-gold complex and is carried up to the patient test result region
  • the antibody-HCG-gold complex reaches the test region and binds to immobilised antibodies here that are specific to the antibody-HCG gold complex
  • A coloured line develops
  • A positive control also is run where the monoclonal antibodies without HCG bind to the immobilised antibodies, causing a colour change
103
Q

What are anabolic steroids?

What do they do?

How can they be bad?

How are they tested for?

A
  • Molecules similar to the sex hormones
  • Stimulate anabolic reactions in the body
  • Lipid soluble so can directly effect protein synthesis at the level of the gene
  • Can cause aggression, increase muscle size and strength mimicing action of male sex hormone testosterone
  • They can be detrimental to health, reducing natural hormone production, suppressing the immune system and causing liver damage
  • Urine is randomly tested by gas chromatograph and mass spec in athletes for the presence of steroids or their intermediates
104
Q

What extra thing can happen at the collecting duct when there is a very low water supply?

A
  • cells at the base of the collecting duct become permeable to urea which diffuses into medullary tissue contributes to decreasing water potential so more water diffuses out of urine before enters pelvis.
  • stimulates by ADH
105
Q
  1. What is photosynthesis?
  2. where does it take place?
A
  1. process where light energy from the sun is converted into chemical potential energy that cna be used to synthesise complex organic molecules like glucose (anabolic metabolic mathway where energy is used up (endothermic) to produce glucose and oxygen)
  2. the chlorophyll in chloroplastas upper epidermis
106
Q

Why is photosynthesis important?

A
  1. need glucose for respiration to produce ATP for enrgy for metabolic processes like growth
  2. oxygen required for breathing
  3. plants provide raw materials like cotton and medicine
  4. animals eat plants, so life depends on them directly or indircetly as an energy source
  5. human food industry, agriculture and livestock farming
107
Q

What is the theory of how photosynthesis evolved?

What is the evidence?

A

evolved in free living prokaryotes and were taken into eukaryote cells by endosymiosis

Evidence:

  1. Chloroplasts only produced form division of other chloroplasts whcih is seperate from plant cell division
  2. have their own genome with circular loop of DNA like prokaryotes
  3. Have their own 70s ribosomes and protein synthesis mechanism
  4. contain similar pigments to photosynthesising cyanobacteria
108
Q

Where does the light dependent stage occur?

Where does the light independent stage occur?

A

Thylakoid membranes

Stroma

109
Q

Autotrophs

Examples of types of autotrophs

A

synthesise complex organic molecules from inorganic molecules and an energy source. can photosyntheise

  • Chemoautotrophs- such as nitrifying bacteria oxidise ammonia to nitrite
  • Photoautotrophs- such as plants use light and co2 to create sugars and then complex carbohydrates
110
Q

Heterotrophs

A

Fungi, animals and some bacteria can’t synthesise their own food and need to ingest complex organic molecules which they digest into smaller, soluble ones that can be used as building blocks for creating their own large complex molecules

(obtain complex organic molecules by eating other organisms)

111
Q

Chloroplast structure

A

2-10 micrometers

intergranal lamellae

inner membrane- has transport proteins to allow certain chemicals and control of movement between cytosol and stroma

outer membrane- allows small ions and molecules into chloroplast

starch grain- contains starch molecules produced from sugars made in photosynthesis- energy store

lipid droplet- made from sugars produced in photosynthesis and store energy. can be used for fatty acid synthesis and phospholipids

stroma- contains enzymes for calvin cycle. surrounds grana stacks so its easy to transfer products of dependent to independent

thylakoid membrane- embedded with chlorophyll molecules and electron carriers and ATP synthase enzymes for light dependent reactions

granal stacks- increase SA of thylakoids allowing many photosystems to be present for maximum light absorbance

112
Q

What are photosynthetic pigments?

A

found in the thylakoid membranes, they are molecules that absorb light energy (from the visible part of the electromagnetic spectrum)

there are several different pigments, each absorbing different wavelengths so more can be absorbed

113
Q

Names of photosynthetic pigments

what they reflect and absorb

what colour they apear

What wavelength they absorb

A

Chlorophylls:

chlorophyll a:

  • (p680 and p700)
  • abrorb red and blue- violet light
  • reflect green
  • appear yellow- green

Chlorophyll b:

  • absorb 500nm and 640nm
  • appears blue green

Carotenoids:

  • reflect yellow and orange
  • absorb blue- violet
  • appear yellow, orange, red and brown
  • usually masked by green chlorophyll but can be seen prior to leaf fall since chlorophyll breaks down first
  • EG carotene, xanthophyll
114
Q

What are photosystems

A
  • funnel shaped clusters of photosynthetic pigments held in place by protein complexes in the thylakoid membrane. made of light harvesting system and pprc
  • in the light harvesting system, accessory pigments capture light energy and transfer it to the primary pigment recation centre
  • chlorophyll a is in the pprc and carotenoids and clorophyll b are accessory pigments
  • this allows maximum light absorption
115
Q

Structure of chlorophyll

where are the types of chlorophyll a found

A

consists of a porphyrin ring containing mg and a hydrocarbon chain

p680 absorbs light maximally at 680nm wavelength in PS2

p700 absorbs light maximally at 700nm and is in PS1

116
Q

Absorbtion spectrum v action spectrum

A
117
Q

Where are PS1 and PS2 located?

A

PS1- integranal lamellae

PS2- granal lamellae

118
Q

Non cyclic photophosphorylation

A
  • electrons excited from pS2 instead fo returning to PS2 at the end fo the electron transport chain, they replace the lost electrons from PS1
  • ATP is produced by chemiosmosis
  • electrons emitted from PS1 pass down another electron transport chain are used to reduce NADP rather than generate ATP
  • To reduce NADP you need H+ aswell as e-
  • water broken down to replace lost e- from reaction centre of PS2
119
Q

What is photophosphorylation?

A

the process of usign light enrgy to synthesise ATP from ADP and inorganic phosphate when a high energy electron passes through an electron transprt chain in the thylakoid membranes

120
Q

What is photolysis?

A

PS11 contains an enzyme that splits water molecules when it is activated by light

2H20–> 4H+ + 4e- + O2

The hydrogen ions are taken up by the NADP and then combine with electrons from PS1

the electrons produced replace lost electrons from PS11

121
Q
A
  1. Thylakoid membranes are impermeable to H+
  2. As the e- are passed down the ETC, the carriers transport H+ into the thylakoid space against the concentration gradient. requires energy gained from the ETC
  3. a positive charge builds a proton motive force
  4. ATP synthase proteins allow H+ to pass through back to the stroma and synthesise ATP at the same time
  5. approximately 3 H+ are needed for every ATP made
  6. the H+ are then available for the reduction of NADP
  7. this is the chemiosmotic hypothesis
122
Q

Cyclic photophosphorylation

A
  • only involves PS1 when need more ATP
  • results in the formation of ATP but not reduced NADP
  • light is absorbed by the photosystem and the energy is passed onto chlorophyll a in the reaction centre
  • this excites the electron enough for it to leave the chlorophyll molecule and enter an electron transport chain
  • as it moves down the chain the energy released is used to synthesise ATP
  • once the electron has lost all its energy it returns to PS1
  • PS1 can still produce ATP without e- from PS11
123
Q

where are the products for the light independent reactions obtained from?

A

occur in the stroma via a cyclic pathway called the calcin cycle

uses CO2 diffused in through open stomata, into the air space, intercellular spaces in the spongy mesophyll, palisade mesophyll, thin cell wall, cell membrane, cytoplasm, chloroplast envelope, stroma

ATP and reduced NADP from the dependent stage

124
Q

Summary of the stages of the calvin cycle

A

Fixation/ carboxylation

  • In the stroma CO2 is fixed by the 5C compound ribulose bisphosphate (RuBP)to form an unstable 6C compound.
  • RuBP is a CO2 acceptor molecule.
  • This process is catalysed by the enzyme RUBISCO and is a carboxylation reaction
  • RUBISCO is made in chloroplasts using chloroplast DNA
  • The 6C compound immediately splits into two molecules of a 3C compound called glycerate-3-phosphate (GP).

Reduction

  • ATP and reduced NADP from the light dependent stage are used to reduce glycerate-3-phosphate to produce triose phosphate (TP –a 3c phosphorylated sugar)

Regeneration

  • One sixth of TP is used to make glucose, amino acids, fatty acids, glycerol or nucleic acids.

Five sixths are used to regenerate more RuBP (this also requires ATP).

  • Therefore the cycle repeats 6x to make glucose
  • 12TP molecules made in 6 cycles, 2 removed to make glucose. 10 recycled to generate 6 RuBP
  • 10x3 carbon TP = 30 carbons. this means 6 5 carbon RuBP
125
Q

Uses of calvin cycle products

A
  1. •GP can be used to synthesise fatty acids by entering the glycolytic pathway and being converted to acetyl Co A
  2. •TP is used to synthesise glycerol
  3. •GP and inorganic salts are used to synthesise aa
  4. •Pairs of TP combine to form hexose sugars e.g. glucose
  5. •Glucose and fructose combine to form sucrose the main translocatory sugar
  6. •Starch is synthesised in the stroma for energy storage
  7. •The structural carbohydrate cellulose is also synthesised
126
Q

inputs and outputs of thr light dependent and independent stages

A

Dependent:

Input-

  1. light
  2. H20
  3. ADP
  4. Inorganic phosphate
  5. Oxidised NADP

Output-

  1. O2
  2. reduced NADP
  3. ATP

Independent:

Input-

  1. co2
  2. ATP
  3. reduced NADP

Output-

  1. lipids
  2. glucose
  3. aa and fatty acids
  4. oxidised NADP
  5. inorganic phosphate
  6. ADP
127
Q

What is a limiting factor?

A

A limiting factor is the factor that is available in the lowest or least favoured value and so will limit or restrict the rate of a metabolic process.

128
Q

What factors affect the rate of photosynthesis?

A
  1. light intensity
  2. conc of CO2
  3. temperature
  4. not water as for water pot. to be low enough to limit RO photosynthesis the plant will have already closed its stomata and stopped photosynthesis

chlorophyll is the ultimate limiting factore

129
Q

How does light affect the rate of photosynthesis?

A
  1. for energy source to excite electrons in photophosphorylation.
  2. energy for photolysis of water. i
  3. ncreased intensity means ATP and reduced NADP produced at an increased rate, so more GP to reduced TP so more ATP for regeneration of RUBP.
  4. causes stomata to open so CO2 can enter.
130
Q

How does carbon dioxide concentration affect the rate of photosynthesis?

A
  • source of carbon so increases rate of carbon fixation in calvin cycle and rate of TP production.
  • 0.04% conc in atmopshere.
131
Q

How does temperature affect the rate of photosynthesis?

A
  1. affects rate of enzyme controlled reactions until denaturation. eg carbon fixation.
  2. also photorespiration at a higher temperature above 25 degrees even if not denatured. At high temps rubisco catalyses a reaction combining oxygen with RuBP instead of CO2. It means that the oxygenase activity of rubisco exceeds the carboxylase activity. ATP and reduced NADP are produced and wasted as photorespiration exceeds photosynthesis. competitive inhibition.
  3. Every 10 degree rise in temp, rate doubles up to 25 degrees. higher temperature means more kinetic energy and increased frequency of successful collisions and ROR. Increased conc. of GP, TP, RuBP
  4. increased temperature increases water loss due to transpiration. this leads to stress response, so stomate close and CO2 uptake is reduced so is photosynthesis.
132
Q

How does light intensity affect the products of photosynthesis?

A
  • light dependent stage stops
  • reduced quantitiy of ATP and reduced NADP
  • GP increases
  • TP and RuBP decrease
133
Q

How does carbon dioxide concentration affect the products of photosynthesis?

A

low concentration of GP and TP

RuBP increases as still formed from TP but not being used to fix CO2

can be supplied by sodium hydrogen carbonate

134
Q

A4 diagram page on photosynthesis

A
135
Q

Why respire

A
  • active transport- essential for uptake of nitrates by root hair cells, loading sucrose inot sieve tube elements, selective reabsorbtion of glucose and aa in kidney, conduction of nerve impulses
  • anabolic reactions- building of polymers like proteins, polysaccharides, nucleic acids essential for growth and repair
  • movement by cilia, falgella, or contractile filaments in muscle cells
136
Q

What is a tropism?

A

a growth response to a stimulus

137
Q

Hydrotropism

A
  • response to moisture
  • root tips grow towards damp areas of soil increasing access to water
138
Q

Chemotropism

A
  • response to certain chemicals
  • pollen tubes grow around the flower stigma towards the ovules
139
Q

Phototropism

A
  • shoots have a positive phototropism so maximum light for photosynthesis
  • when tip is lit form 1 side the auxin moves to the far side away from the light. The cells then elongate more on the dark side so the tip curls towards the light
  • the root is negatively phototropic so grows away from light towards the soil after a heavy period of rain
140
Q

How does auxin cause growth?

A
  • Indole-3-acetic acid (IAA) is an auxin synthesised in the meristem and passes down the stem
  • stimulates proteins in cell wall called expansins to make the cell wall more flexible
  • the vacuole expands by uptake of water and cytoplasm pushes against cell wall
  • it also binds to receptor sites in plant cell membrane causing pH to fall to 5 which is the optimum temp for enzymes keeping the cell wall flexible
  • as cells mature, auxin is destroyed and pH rises so enzymes become inactive, cell walls become rigid and stop growing
141
Q

What plant is used for tropism experiments and why?

A
  • Often use germinating seeds and young seedlings as easy to manipulate as they are growing and responding rapidly so any changes show up quick
  • Changes also tend to show up on whole organism so tropisms easier to measure
  • Seedling of monocotyledonous plant like cereals used so shoot emerges as 1 spike known as cleoptile
  • However, responses of adult plant may be more complex
142
Q

What was Darwins experiment and what did it show?

A
  • When the tip of a coleoptile (sheath surrounds young shoot in grasses) Was removed there was no response to unidirectional light
  • This indicated the tip was responsible for detecting light
143
Q

What was Boysen Jensen’s experiment and what did it show?

A
  • When the cup tip was replaced with the gelatin barrier inserted the phototrophic response was restored.
  • This indicated the stimulus for growth was a chemical as chemicals would travel through the barrier not electrical
  • The second experiment used a mica barrier which is impermeable to chemicals. It was only inserted halfway through the coleoptile either on the side where light was or wasn’t. When the Barrier was on the lit side they bent towards the light but when on the side without the light there was no response
  • This meant the signal was a chemical (hormone) and was produced in the tip and travel down on the side opposite to the stimulus. It also meant that the stimulus acted by causing growth on the unlit side not inhibiting growth on the lit side
144
Q

What is different about plant hormones?

A
  • they arent produced in specific organs but may be produced in a restricted region
  • they are produced by unspecialised cells and the effect on plants may be different in different circumstances
145
Q

What happens to plants growing in the dark?

A

Plants grow more rapidly in the dark because they grow rapidly upwards to reach the light to photosynthesise. When it gets light upwards growth is slowed so that resources can be used for synthesising leaves, strengthening stems and growth.

146
Q

Geotropism

experiment

A
  • negative geotropsim in plant stems when auxin accumulates on lower side, increasing growth, increasing growth on that side so stem grows up
  • positive geotropsim in roots but auxin sccumulates on lower side but inhibits growth so root tips grow down for minerals, water and support

Experiment- plants grown on a rotating drum called a clinostat so the gravitational stimulus is applied evenly to all sides of the plant and the root and shoot will grow straight (in dark)

Or seeds placed in petri dishes and stuck to wall of lab and dishes rotated st 90 * at intervals. Can see response in 2 hrs

147
Q

Apical dominance

experiment

A
  • auxin also prevents lateral side buds as it is made in cells at root tip and moves away down stem and up root
  • lateral shoots grow more further down where auxin concentration is lower
  • is done because its best to grow towards the light for photosynthesis
  • if apex is removed then auxin is removed so lateral side buds grow and curl up towards the light

Experiment where the cut tip is immediately replaced with an agar block containing auxin and inhibition of lateral growth is restored.

148
Q

Chemical defences to repel herbivores

A
  1. tannins
  2. alkaloids
  3. pheromones
  4. terpenoids
149
Q

What are tannins and what do they do?

A
  • water soluble carbon compounds stroed in plant vacuole
  • break down to produce toxic chemicals
  • bitter taste repels herbivores
  • toxic to insects
  • eg tea and red wine
150
Q

What are alkaloids and what do they do?

A
  • nitrogenous compounds derived from amino acids
  • bitter tasting and toxic
  • can affect metabolism and poison animals
  • eg caffiene and nicotene
151
Q

What are pheromones and what do they do?

A
  • chemicals released from 1 member of a species and affect the behaviour/ physiology of another member of the same species
  • eg. ethene causes ripening of nearby fruit
  • eg. maple tree attacked by insects releases a pheromone absorbed by leaves on other branches so they maje chemicals like tannins to protect themselves
152
Q

What are terpenoids and what do they do?

A
  • often from essential oils
  • can acts as toxins for insects and fungi
  • eg citronella from lemon grass acts as an insect repellent
153
Q

Thigmotropsim

A
  • response to touch
  • mimose pudica contains alkaloid and stem has sharp prickles
  • when leaves touched they fold down and collapse to frighten off larger herbivores and dislodge smaller insects
  • the leaf falls in a few seconds and recovers over 10 minutes as K+ ions move into cells followed by osmotic water movement
154
Q

response to abiotic stress

A
  • produce chemicals acting as antifreeze preventing crystals destroying cells and cytoplasm and vacuole sap contains solutes with lower freezing point
  • drought close stomata and loose leaves
155
Q

Leaf loss

A
  1. falling levels of light cause auxin to fall so leaf produces ethene
  2. ethene switches on genes to stimulate breakdown of cell walls abscission layer by enzymes. the abscission layer is a layer of parenchyma cells at the bottom of the leaf stalk with thin walls so are easily broken
  3. the seperation layer is outside the abscission zone and fatty material is deposited here forming a protective scar on the stem side preventing pathogen entry
  4. vascular bundles are sealed
  5. cells in the seperation zone retain water and swell putting strain on weakened outer layer and then abiotic factors cause the leaf to fall

auxin inhibits leaf loss and are produced by young leaves making them insensitive to ethene. auxin concentration decreases as leaves get older

156
Q

Why do plants loose their leaves?

A
  • Deciduous plants loose the leaves when its very hot and dry to reduce water loss and also when it’s very cold and absorption of water can be hard and frozen soils in temperate climate.
  • Here is also limited photosynthesis due to reduce light and temperatures.
  • When glucose required for respiration to maintain leaves and produce chemicals from chlorophyll that may protect them against freezing is greater than glucose produced by photosynthesis.
  • Trees in leaf are also more susceptible to damage.
157
Q

Stomatal closure

A
  • ABA (abscisic acid) produced in roots in response to decreased sool WP
  • is then translocated to leaves where it affects guard cells
  1. ABA binds to receptors on CSM of guard cells
  2. complex series of events results in opening of calcium channels causing Ca2+ ions to enter cytoplasm. pH raised
  3. this causes K+ ions, NO3- and Cl- ions to leave the cell
  4. WP of cell increases so water osmoses out into surrounding cells and loss of turgour causes stomata to close
158
Q

Seed germination

A
  1. when seed absorbs water the embryo is activated and begins to produce giberellins
  2. giberellins stimulate seed germination and the breaking of dormancy by triggering the mobilisation of food stores in a seed.
  3. switches on genes for amylases and proteases so starch stored in endosperm can be broken down providing energy for growth and glucose for respiration
  4. embryo plant uses food stores to produce ATP for building materials for growth

ABA maintains dormancy by inhibiting production of amylase and inhibiting growth

Auxins produced early in germination stimulate growth but higher concentrations inhibit germination

159
Q

Why are they plant hormones not plant growth regulators?

A
  1. not all hormones responsible for plant growth
  2. hormones are chemical messengers
  3. role in cell communication
  4. target cell
  5. wide range of effects
  6. long term effects
160
Q

Commercial uses of plant hormones

A
  1. auxins used as selective weed killers as high concentration causes rapid growth damaging tissue and easy entrance of pathogens. unsustainable growth causes death. cereals and lawns as grasses less sensitive.
  2. lower levels fo auxin can be used as root powders to stimulate growth in cuttings to grow new plants
  3. ethene stimulates fruit ripening by triggering a series of chemical reactions like increased respiration rate. reduce transport damage and reduce waste
  4. Auxins and gibberellins can be used to treat unpollinated flowers causing them to develop seedless fruits (parthenocarpic)
  5. auxins can be sprayed on fruit to inibit abscission to prevent rot when drop
  6. Gibberellins can delay the ripening of fruit to improve the size and shape of fruits
161
Q

Root tip phases

A

zone of cell differentiation/maturation

zone of cell elongation

zone of cell division (root tip)

162
Q

Experiment showing effect of giberellins on stem elongation

Experiment showing effect of giberellins on seed germination

A
  • Experiment- Giberellins were produced by a fungus from the genus giberella that affects rice. The infected seedling grew very tall and thin. Experiments showed plants produce the same compound, and short stemmed plants produce few/ none.
  • Shorter stems reduce waste and make them less vulnerable to damage by weather and harvesting.
  • Mutant strains of seedsbred without gibberellin gene don’t produce gibberellins but can be induced to Germinate if gibberellins are applied
163
Q

Synergism

Antagonism

A

Synergism is the relationship between two factors whether action together is greater than of the separate effects added together. This is how gibberellins work with auxins to stimulate stem growth.

Antagonism is when the substances have opposite effects

164
Q

Photoperiodism

A

is when plants are sensitive to the lack of light. This is due to pigment phytochrome which has 2 forms, and the ratio of its forms changes depending on light levels

165
Q

Practical investigations into the effect of plant hormones on growth.

Why can it be hard to measure hormones?

A
  • Grow in serial dilutions of hormones
  • applying different concentrations of hormones to cut ends of stems or roots and observing the effects
  • use a large number of plants and use standard deviation to measure the spread of data
  • Work in low concentrations so isolating and measuring changes in concentrations is hard
  • Also multiple interactions between different chemical control systems makes it hard to isolate the role of a single chemical in a specific response
166
Q

Summary of roles of plant hormones

A

Auxin

  1. phototropism
  2. geotropism
  3. growth
  4. apical dominance
  5. inhibits leaf loss

Giberellins

  1. seed germination
  2. flowering
  3. cell elongation
  4. cell division
  5. stem growth
  6. delay fruit ripening

Ethene

  1. leaf abscission
  2. fruit ripening

ABA

  1. stomatal closure
  2. maintains seed dormancy
167
Q

what are sensory receptors?

A

specialised cells that can detect changes (stimuli) in our surroundings. They convert a form of energy into the electrical energy that is a nerve impulse so are called transducers.

168
Q

Receptors and stimulus detected:

  1. Photoreceptors (rods and cones) in the retina
  2. Olfactory chemoreceptor cells lining the nasal cavity
  3. Osmoreceptors
  4. Chemoreceptors in mouth
  5. Pressure receptors (Pacinian corpuscles) in the skin
  6. Mechanoreceptors in the cochlea
  7. Muscle spindles (proprioceptors)
  8. Nociceptors
  9. Baroreceptors
A
  1. Light intensity and wavelengths
  2. Presence of volatile chemicals
  3. Concentration of body fluids
  4. Presence of soluble chemicals
  5. Pressure on the skin
  6. Vibrations in the air causing mechanical strain and stretch
  7. Length of muscle fibres indicating body position
  8. Damage sensed as pain
  9. Detect BP
169
Q

Nerves and neurones

A

Nerves are made of many nerve cells each called neurones

Neurones- specialised nerve cells which transmit electrical impulses rapidly around the body so an organism can respond to changes in internal and external environment

170
Q

Sensory neurones:

where do they carry impulses?

Where are their cell bodies?

What do the cell bodies contain and why?

What is the name of the main body?

A

Carry impulses via long dendrons from the sensory receptor to the brain or spinal cord

Their cell bodies are in structures called dorsal root ganglia just outside the spinal cord

All cell bodies contain a nucleus and many mitochondria and ribosomes involved in production of neurotransmitters

After the cell body the dendron is known as the axon

171
Q

Motor neurones:

Where is the cell body?

Where do they transmit messages?

what does each end connect to?

A

Cell body is in the CNS at the end

Transmits messages from the CNS to an effector

The axon takes impulses away from the cell body to the motor end plate which synapses with an effector (muscle or gland)

Dendrites connect to other neurones and conduct impulses into the cell body

172
Q

Difference between sensory and motor neurone?

A
  • Cell body is not at the end of the cell, its in the middle at dorsal root ganglia
  • Cell body at one end of cell in CNS
  • Cell body does not have dendrites
  • Cell body has dendrites
  • Impulse travels towards CNS from a sensory receptor
  • Impulse travels away from the CNS to the effector
  • Axon terminal connects to other neurones in CNS or directly to motor neurone
  • Axon terminal transmits impulses to effectors
  • Dendron and axon
  • No dendron, only axon
173
Q

Similarities between sensory and motor neurone?

A
  1. All cell bodies contain a nucleus, many mitochondria and ribosomes
  2. Both have axon
  3. Both have axon terminal
174
Q

Where is the relay neurone and what is its structure?

A
  • Between sensory and motor neurones in the CNS
  • Many short axons and dendrons
175
Q

What is the axon surrounded by?

What is the sheath made of?

What does it do?

How do the cells form?

What are the gaps called?

A
  • The axon is surrounded by a myelin sheath formed by several Schwann cells
  • The sheath is mainly lipid and some protein
  • It electrically insulates the axon
  • Schwann cells wrap an elongation of their plasma membrane several times around the axon
  • Each time they grow around a double layer of phospholipid bilayer is laid down
  • The gaps between the cells are Nodes of Ranvier
176
Q

Relfex arc

A
  • Gives a rapid response
  • No conscious involvement of the brain
  • The response is the same each time
  • It protects the body
177
Q

Pacinian corpuscle

A

The end of the sensory neurone is found within the centre of the corpuscle surrounded by layers of connective tissue called lamellae. Each layer of connective tissue is surrounded by a layer of gel

Within the membrane of the neurone there are sodium ion channels. The ones ending in the Pacinian corpuscle are called stretch mediated sodium channels, as when they change shape their permeability to sodium also changes.

178
Q

How does the Pacinian corpuscle convert mechanical pressure into a nervous impulse?

A
  1. Resting state, the stretch mediated sodium ion channels in the sensory neurones membrane are too narrow for sodium to pass through. The neurone has a resting potential.
  2. Pressure applied to corpuscle it changes shape of lamellae causing membrane surrounding its neurone to stretch

Sodium ion channels present widen so sodium ions can diffuse into the neurone

4.The membrane potential changes and it becomes depolarised, resulting in a generator potential

The generator potential creates an action potential (nerve impulse) that passes along the sensory neurone

179
Q

What channels are in the neurone membrane?

A
  • There are protein channels and K+ and Na+ ions, which are voltage gated and usually closed but K+ leaks out as open
  • Also antiport active transport pump for K+ and Na+
180
Q

resting potential

A
  • When a neurone isn’t transmitting an impulse the pd across the membrane (difference in charge between inside ad outside of axon) is the resting potential.
  • It is still involved in active transport, where Na/K pumps remove 3Na+ ions from the neurone and 2K+ ions in
  • The plasma membrane is more permeable to potassium ions than sodium ions so some of the potassium that was pumped in leaks out
  • Here the outside of the membrane is more positively charged than the inside.
  • The membrane is polarised as there is a pd of -70mV across it.
181
Q

Generation of an action potential

A

1. Resting potential of -70mV

  • Polarised
  • 3Na+ ions out, 2K+ ions in
  • Na channels closed, K+ open so leakage out
  1. Generator potential
  • Some Na+ ion channels open so start to diffuse into the cell
  • Membrane potential becomes less negative
  • The bigger the stimulus the more gates open and the more generator potentials form
  1. Threshold potential reached by membrane potential and an action potential is propagated
  • Stimulates the opening of Na+ ion voltage gated channels (positive feedback)
  • Rapid influx of Na+ ions by facilitated diffusion into cell
  • Depolarisation as inside becomes more positive than outside
  1. Membrane is depolarised
    * All sodium ion voltage gated channels close at +30Mv – stimulus
  2. Stimulus of K+ ion voltage gated channels to open
    * Rapid efflux of K+ ions out of cell by facilitated diffusion
  3. Repolarisation of membrane potential as pd reduced
  4. Hyperpolarisation
    * Membrane potential becomes more negative than resting potential so stimulates close of k+ ion voltage gated channels
  5. Sodium potassium pump returns membrane potential to resting potential
182
Q

Generator potential

A
  • This depolarisation is self-perpetuating- once it starts it continues all along the neurone membrane
  • Size of action potential along a neurone doesn’t change regardless of strength of stimulus
  • It either occurs or it doesn’t- ALL OR NOTHING LAW
  • Higher stimulus= higher frequency
  • Also may stimulate more neurones in a nerve
183
Q

refractory periods

A

Absolute refractory period

  • During an action potential a second stimulus will not produce a second action potential no matter how strong that stimulus is
  • Corresponds to the period when the sodium channels have opened and are then closed and inactive and most potassium channels are open
  • This ensures action potentials are unidirectional as prevents action potential propagation backwards too. Also ensures action potentials don’t overlap and occur as discrete impulses

Relative refractory period

  • Another action potential can be produced but only if the stimulus is greater than the threshold stimulus
  • Corresponds to the period when the many sodium channels are closed and still inactive and a few potassium channels are still open and the hyperpolarised period
  • The nerve cell membrane becomes progressively easier to stimulate as the relative refractory period proceeds
184
Q

Transmission of action potentials

A
  • The myelin is impermeable to ions so ion exchange and hence action potentials only occur in the nodes of Ranvier
  • There tends to be few voltage gated channels where the myelin is
  • Transmission of an action potential is by rapid saltatory conduction
  • Localised circuits
  1. Where an action potential occurs at one point in a neurone Na+ ions enter
  2. This disturbs the ionic balance set up by the Na/K pump
  3. As the Na+ concentration increases inside the neurone Na+ start to diffuse down the axon down concentration gradient
  4. This changes the pd further down the axon making it less negative so -55mV (over threshold) and opens Na+ gates to let Na+ in causing depolarisation and initiate another action potential
  5. The Na+ then diffuses to next node and the pump returns to normal- repolarisation
  6. At the end it synapses with another nerve
185
Q

Unmyelinated v myelinated sheath

A
  • Unmyelinated must diffuse all the way along so much slower
  • Faster as less places for channels to open and ions to move
  • More energy efficient as repolarisation uses ATP in the sodium pump
  • Unmyelinated neurones often found in grey matter of CNS where axon is short and doesn’t have to transmit impulse far
186
Q

What other factors affect the speed of an action potential?

A
  1. Speed increases with axon diameter and myelinated are thicker as less resistance to the flow of ions in the cytoplasm
  2. Higher temperature makes nerve impulse move faster as ions diffuse faster. Up to 40 degrees as higher temperatures denature proteins like sodium potassium pump
187
Q

Role of synapses

A
  1. Allow transmission of impulses between neurones
  2. Synapses ensure unidirectional transmission in the synapse so signals are directed along specific pathways only as receptors only on postsynaptic side
  3. Allows for different neurones to diverge from different pathways e.g. one presynaptic diverges to several post synaptic neurones/Several presynaptic neurones converge on 1 post synaptic neurone so different stimuli create the same effect
  4. Building synapses is the basis of memory and learning
  5. Synapses run out of vesicles after repeated stimulation and become fatigued. This avoids overstimulation and protects an effector or allows acclimatisation to a stimulus
  6. (Low level stimuli can be filtered out at a synapse or summated)
188
Q

What can summation do?

What is spatial summation?

What is temporal summation?

A
  1. Low level signals can be filtered out because they do not generate enough vesicles of neurotransmitter to be released to generate an AP in the postsynaptic neurone
  2. Low level signals can be magnified by summation of which there are 2 types

Spatial summation

When excitatory potentials from many different presynaptic neurones cause the postsynaptic neuron to reach its threshold and fire

Temporal summation

When a single presynaptic neuron fires many times in succession, causing a postsynaptic neurone to reach its threshold and fire

189
Q

Synaptic transmission

A
  1. Action potential arrives at the synaptic knob of the pre-synaptic neurone
  2. Depolarisation of membrane stimulates opening of calcium ion voltage gated channels, so calcium diffuses into the synaptic knob
  3. Ca2+ ions stimulate vesicles containing neurotransmitters to migrate and fuse with presynaptic membrane
  4. Neurotransmitters released into synaptic cleft by exocytosis. They diffuse across synaptic cleft where it binds to receptors on post synaptic membrane
  5. Binding stimulates opening of sodium ion channels, so they diffuse into post synaptic neurone. Post synaptic membrane starts to depolarise.
  6. Once threshold potential reached Na+ ion voltage gated channels open and an action potential is generated passing down the post synaptic neurone
  7. Neurotransmitter released from receptors are either taken back to synaptic knob to be reused r broken down by an enzyme. Then it’s taken back to the synaptic knob to be rebuilt into a neurotransmitter and reused. Prevents restimulation and allows another stimulus to arrive
190
Q

Example of synaptic transmission

A

Eg. Cholinergic synapse

Neurotransmitter- acetyl choline

Enzyme- acetyl cholinesterase

Hydrolysed to choline and ethanoic acid

Common in the CNS of vertebrates and where motor neurone and muscle cell meet- neuromuscular junctions causing muscle to contract

191
Q

Types of neurotransmittter

examples

A

Inhibitory synapses

These neurotransmitters result in the hyperpolarisation of the postsynaptic membrane preventing an action potential being triggered. Instead of causing sodium channels to open, they cause chlorine ones to open which are negative. This means a bigger stimulus is needed to reach the threshold.

Eg. Gamma-aminobutyric acid (GABA) is found in some synapses in the brain

Excitatory synapses

These neurotransmitters result in the depolarisation of the post synaptic neurone. If the threshold is reached in the postsynaptic membrane an action potential is triggered.

Eg. Acetylcholine

192
Q
A

Biology (6 decks)

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