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258 - physiology > lecture 6+7:summary oxidative, Regulation of the ETC and start of blood glucose > Flashcards

lecture 6+7:summary oxidative, Regulation of the ETC and start of blood glucose Flashcards

1
Q

what is the process of ETC and energy made called

A

oxidative phosphorylation

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2
Q

what are the 4 points of summary of oxidative phosporylation

A

1) electron transport (in pairs) down the ETC from MADH or FADH2
2) Complex 1, 3 and 4 pump protons out of mito matrix to the intermembrane space (against a gradient, get energy from the electrons)
3) the pumping of the protons (h) cause a high concentration of protons and an electrical potential=electrochemical gradient
4) the H+ flow back into the matrix through ATP synthase drives atp synthesis

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3
Q

when hydrogen protons are pumped into the intermembrane space , is it down or against their chemical gradient

A

against their concentration gradient which is why they need energy from electrons

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4
Q

explain the general carbon flow for glycolysis

A

glucose (6C) > 2 pyruvates (3C)

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5
Q

How many NADH do you form from glycolysis

A

2 NADH

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6
Q

What is the ATP produced for glycolycis (without oxydative phos)

A

2 atp

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7
Q

What is the ATP produced for glycolis (with oxydative phos)

A

2 NADH molecules made from glycolysis go into oxidative phos. and make 6 atp total

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8
Q

what is the total theoretical yield for glycosis (with ETC)

A

8 atp

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9
Q

what is the general carbon flow for the pyruvate oxidation

A

2 pyruvates (3 carbon) > 2 acetyl coa (2 carbon)

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10
Q

how many NADH are produced from pyruvate oxidation

A

2 nadh (1 per pyruvate)

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11
Q

what is the atp yield for just pyruvate oxidation (wihtout ETC)

A

none

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12
Q

what is the yield of atp from pyruvate oxidation going to ETC

A

2 NADH go into ETC

6 atp are made

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13
Q

what is the total theoretical yield for pyruvate oxidation

A

6 atp

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14
Q

wht is the general carbon flow for kreb cyclem

A

2 acetyl coa (2 C) > 4 CO2

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15
Q

how many nadh and fadh2 are producted in the kreb cycle (for 2 acetyls)

A

6 nadh

2 fadh2

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16
Q

what is the atp yield solele from kreb cycle (without ETC)

A

2 atp

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17
Q

what is the atp yield for kreb cycle going into ETC only

A

6 nadh will give you 18 atp

2 fadh2 will give you 4 atp

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18
Q

what is the total theoretical yield for kreb cycle (with etc and alone)

A

24 atp

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19
Q

what is the general carbon flow for areboic glycolysis (everyhing together)

A

glucose (6 C) > 6 CO2

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20
Q

what is the total FADH2 and NADH made from all 3 processess (glycolysis, pruvate oxi and kreb)

A

10 nadh

2 fadh2

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21
Q

what is the net atp yield from substate phosphoraltion of all 3 processess only

A

4 atp

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22
Q

net atp yield through the oxidative phosphtation of the 3 processes

A

34 atp

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23
Q

what is the net yield maximum of all three processes

A

38 atp

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24
Q

where does the oxygen come from for the ETC

A

comes from circulation

o2 hemoglobin blood

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25
where is CO2 in the 3 different processess
2 co2 for 2 pyruvates to acetly | 4 co2 for kreb cycle
26
what are some different functions for ATP
muscles (contraction) nerve (actvie ion transport) protein building (synthesis of new molecules or cell grouwth and division)
27
what are some ways we can be lacking oxygen for the electron transport
during exercise during high altitude blood circulation problems
28
what is the net atp for anerobic glycolis
2 atp
29
what are the 2 factors taht positively influence the ETC
``` aerobic exercise (training at better oxygen utilization) High intensity interval training (adaptations of mitochondira) ```
30
what are the 4 inhibirors (negatively affect) the ETC
- Cyanide - Olygomyosin - Carbon monoxide - Rotenone
31
what is olygomysion
antibiotic
32
what does CN stand for
cyanide
33
what does CO stand for
carbon monoxide
34
what is rotenone
pesticide
35
which is the least lethal inhibitor of the ETC
carbon monoxide
36
where does rotenone affect and what does it do
inhibits electron transport at complex 1 =block all downstream electron activity (electrons cannot transfer) hydrogens will not be able to go through and atp synthesis will cease
37
where do cyanide and carbon monoxide affect the ETC and how
they inhibit electron transport chain at Complex 4 it does not allow electrons to go to oxygen since no hydrogens can bind with oxygen, oxygen will build up in the cell and will become a radical form which can cause metabolic damage to the mitochondria
38
where does olygomision inhibit the ETC and how
blocks the ATP synthase molecule (inhibits hydrogens from coming back through the membrane so no ATP would be formed
39
what do uncoupler poisins do and give an example
they carry alot of the protons into the matrix (=taking away from intermebrane space ) Heat is going to be formed and REDUCED ATP
40
explain oligomyosin and relationship with cancer
oligomycin is an antibiotic that can be given to cancer patients to kill the mitochondria of cancer cells (but is also killing off a lot of healthy cells) Research is being used to only use the root of it that will kill mostly bad cells but can affect healthy cells like hair)
41
explain the consequence of CN toxicity
CN binds to cytochrome oxidaze (complex 4) which blocks the pairs of electrons causing an increase in pairs of electrons This electron pairing blockage will impede hydrogens from going up (killing electrochemical force) Since there is a buildup of H, FADH2 and NADH concentrations will rise since they cannot be oxidized If there is an increase of FADH2 and NADH, the kreb cycle will be inhibited If the kreb cycle is inhibited, acetyl coa will buildup since it cannot go through the process if acetyl coa builds up , pyruvate is not going to go to acetyl coa and instead will move towards lactate =BUILD UP OF LACTATE =LACTIC ACIDOSIS Also, no electrons will be binding with oxygen cause and increase in free radicals which is damaging to the cell
42
how will increasing the amount of hydrogen in the cell affect ph
ph will decrease and will decrease cell metabolism causing cell death
43
explain lactic acidosis
high levels of lactic acid (brought on by CN binding onto the complex 4) which can poison your cell and decrease oxidative phosphor.
44
what is DNP (name )
2.4 dinitrophenol
45
true or false: DNP can easiliy diffuse though the inner mito membrane
true
46
what is DNP (in terms of poinsin)
uNCOUPLER
47
is DNP lipophillic or hydrophobic
lipophilic (easily diffuse through membrane)
48
What is important about DNP in terms of ints structure
has a spot to bind hydrogen
49
What is the poisin that used to be used for weight loss
DNP
50
Explain the consequence of DNP (in terms of body weight)
DNP binds the hydrogen on itself and diffuses through the membrane (a lot of hydrogen diffuses through) =loss of electrochemical gradient =ATP production will drop significantly DECREASE IN ENERGY CHARGE. AMP concentration in the cell will increase which will speed up glycolysis and lipolysis (breaking down the carbs and fats for energy in the absence of ETC) =loss of body weight Because of the increased breakdown of carbs and fats, FADH2 and NADH will increase which means Electons are still going through even without the ATP production and because of this, heat is being produced in the mitochondria cause the cell temperature to increase =HYPERTHERMIA
51
what are the 2 affects on the mitchondira when you do aerobic training
1) increase the mitochondrial size | 2) increase in mitcondrial number
52
how does an increase in mitochondiral size positively affect ETC
by increase mitochondira size, you are increasing the size of the inner mictohondiral membrane =Electron transport chain will get larger =consume more oxygen, produce far more atp
53
how does an increase in mitochondira number positively effect the ETC
More mitochondrial, you need greater oxygen consumption | with greater oxidative consumption, you will get an increase in number of atp
54
what is the clinical application of aerobic training vs mitchondira
you will need one oxygen and produce more atp | =INCREASE IN VO2 MAX
55
does skeletal muscle have the necessary enzymes to allow glucose to go back into the circulatoon
no
56
what is the enzyme responbible for allowing glucose 6 phospohate to go to glucose in the liver
glucose 6 phosphotase
57
what is the purpose of gluconeogenesis
maintain circulating blood glucose levels by manufacturing glucose from the liver (ie. when you feel hypoglycemic the liver will sense this and produce more glucose in the circulation)
58
what is the chief organ important for maintenace of blood glucose level
LIVER
59
what is normal blood glucose values
4-8 MM
60
what are the 3 precursors to gluconeogenesis
lactate glycerol alanine
61
where does lactate come from to get into circulation
skeletal muscle
62
where does alanine come from to get into circulation
proteins
63
where does glycerol come from to get taken up in circualtion
adipocytes
64
How is alanine important for gluconeogenisis (structure)
Alanine has 3 carbons and a nitrogen group just need to get rid of the nitrogen group and it can become pyruvate which can become glucose 6 phosphate and then help in gluconeogenic
65
true or false, pyruvate can easily turn into glucose 6 phosphate
true
66
what is the process of pyruvate (from diff sources) going to glucose 6 phosphate and then out as glucose called
gluconeogenesis
67
how is glycerol important for gluconeogeneis (structure)
Glycerol can also be taken up into the liver from a different metabolic pathway and become glucose
68
how is lactate important for gluconeogeneis s(structure)
lactate is very similar to pyruvate (same structure with 2 hydrogens added on) therefore it can become pyruvate and then glucose
69
if gluconeogenesis didnt happen, what would happen
we would have no way to maintain blood circulation levels without a food source therefore in periods of rest (like sleep) we would become hypoglycemic
70
what is the reason the precursors to gluconeogenesis can easily turn into pyruvate
they are all 3 carbon based
71
true or false: glycerol enters gluconeogenis at the same place as lactae and adenine
false, higher up

258 - physiology (21 decks)

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