Exam 2 Flashcards
enzyme-substrate complex
- enzyme changes shape to fit substrate
- pepsin (stomach protein); the substrate, a polypetide, is in active site
- machaelis-menton model for E-S complex
optimal temperatures and pH for enzymes
temp: 40 for human, 70 for enzyme from hot spring
pH: pepsin 2.5, trypsin 6.5
-reaction speed
catabolism
process by which we break down molecules into smaller units
-in cytoplasm
process of catabolism
- exergonic- release energy yielding nutrients: C, F, P
2. catabolism breaks it down into energy poor products: CO2, H2O, NH3
energy content
- the driving force is the net change
- count the # of H on the molecule
net change
G of reactants minus G or products
-G: release energy (exergonic)
+G: absorb energy (endergonic)
delta H
change in enthalpy
-loss of heat energy is favored
delta S
change in entropy
-increase in randomness is favored
coupled reactions
- photosynthesis has a positive change in energy content as energy is put in
- Sum’s fusion reaction has a massive negative change in energy content as light energy is released
oxidation reduction
oxidation- loss of electrons
reduction- gain of electrons
releasing energy
- massive explosion (can’t capture energy)
- metabolic pathways
metabolic pathways
- series of steps where each step releases a energy (ATP, NADPH, NADH, FADH2)
- series of enzymes changing the substrate to make product
substrate level phosphorylation
-pyruvate kinase binds PEP and ADP making pyruvate and ATP
NADH
- NAD+ is a coenzyme
- NAD+ and energy rich molecule go into enzyme and a chain of -e and +p is transferred making NADH (redox reaction)
- each in mitochondria membrane produce 2.5 ATP
decarboxylation
removal of CO2 from a molecule
pyruvate oxidation
pyruvate loses CO2 and CoA goes in while NAD+ goes into NADH making acetyl CoA
glutamate
glutamete has an amino group removed making alpha-ketogluterate (amino acid taking amino off and using molecule for energy)
cellular respiration
cells harvest energy by breaking bonds and shifting electrons across molecules
-aerobic and anaerobic respiration
-fermentation
(focus on carbohydrates, especially glucose)
aerobic respiration
final electron acceptor is oxygen
-for anaerobic its not
why glucose
- universal: everything does it
- glucose break down intermediates used for energy, reducing power, and as C skeletons to make other molecules
- central pathway of all biochemical processes
glucose
-main product of photosynthesis
-start point for cellular respiration in prokaryotes and eukaryotes
C6H12O6
glycolysis
- makes 2 ATP per glucose
- activated by glucose
1. C+glucose= fructose diphosphate
2. cleavage and rearrangement= PGAL + DHAP
3. energy harvesting reactions (substrate level phos.)
4. pyruvic acid
activation of glucose
hexokinase and phosphofructokinase
-add phosphates
harvesting energy from glucose
- PGAL makes 2 NADH (redox reaction)
- phosphoglycerate kinase and pyruvate kinase make 4 ATP each (substrate level phos.)
NAD+
removes e- from substrate making NADH, an e- carrier, that feeds e- transport chain in mitochondria
net gain for glycolysis
2 ATP, 2 NADH, 2 pyruvate
releases 52 kcal/mol out of 686 in glucose (2.1%) and 28% of this is captures (plus NADH)
G-6-P crossroad
- loses PO4 to make glucose and leave liver
- pentose pathway- makes NADPH and fat
- G-1-P- makes glycolygen for synthesis and storage
- F-6-P- glycolysis and aerobic respiration (ATP, NADH, and FADH
pyruvate crossroad
- ethanol
- lactate dehydrogenase to make lactate
- oxaloacetate
- acetyl coA
acetaldehyde
use under low oxygen to recycle NADH to NAD+ (makes lactate and ethanol)
lactate
- in no O2, it makes pyruvate into lactate
- accumulated when fatigued
- if high muscle activity, hydrolysis leads to extra H+ (acidic)
Acetyl-6A crossroad
- fatty acid synthesis in cytoplasm
- triglyceride degradation that frees glycerol and fatty acids (cytoplasm)
- citric acid for krebs cycle and aerobic respiration
- makes FADH2 and NADH in mitochondria - beta oxidation- makes FADH2 and NADH and acetyl-coA in mitochondria
oxidation of pyruvate
as pyruvate enters the mitochondrion, it is decarboxylated by pyruvate dehydrogenase
krebs cycle
oxidizing acetyl-CoA
1. priming C2+ C4= C6
2-9. energy extraction
-alpha ketogluterate makes succinyl-coA (makes atp)
-succinate goes through succinate dehydrogenase to make fumerate
-fumerate makes malate which goes through malate dehydrogenase to make oxaloacetate
krebs cycle net gain
for every 2 pyruvate:
- 3 NADH (makes 2.5 ATP)
- 1 FADH2 (makes 1.5 ATP)
- ATP
oxidative phosphorylation
- electron transport (build proton gradient)
- chemiosmosis (exploit proton gradient)
- inner mitochondrial membrane
- NADH feeds 3 complexes and FADH feeds 2
chemiosmosis
- hydrogen goes in to make ATP
- takes 9 for every 1
rotemone
metabolic poison that blocks early in the ETC
-kills fish
cyanide and CO
metabolic poison that blocks ET
DNP
metabolic poison that lets H+ through the membrane
oligomycin
metabolic poison that inhibits ATP synthase by blocking its proton channel (chemiosmosis)
subtracting NH2
glucose= alpha-ketogluterate
asp= oxaloacetate
ala=pyruvate
-intermediary metabolism
intermediary metabolism
connects amino acid and fatty acid (neutral lipids) catabolism to carbohydrates via deamination of amino acids and beta oxidation of saturated fatty acids
- in mitochondrion and cytoplasm (Catabolism)
- products are NH3, H2O, CO2
feedback inhibition
when all have high levels of ATP and NADH, Krebs cycle and fatty acid break down are inhibited
- glycolysis is also inhibited by ATP inhibiting pfk
- allosteric control
feedback inhibitors
- Atp inhibits hexokinase (hexokinase b4 F-6-P)
- AMP and ADP activate pfk
- citrate and atp (krebs cycle) inhibits pfk
- NADH and acetyl coA inhibits pyruvate dehydrogenase
- acetyl-coA activates pyruvate carboxylase
allosteric control of fatty acids
lots of atp shuts down beta-oxidation
-cant even get into mitochondria
breakdown
amino acids- deamination
sugars- glycolysis
fatty acids- beta oxidation
digestion
- hydrolysis of complex molecules to their component building blocks
- conversion of building blocks to acetyl coA
macromolecule intake
protein 15%
fats 20%
carbs 65%
L isomer
amino acids
- protein can be both but we use L
- essential and non essential
lipids
- linoleic fatty acid (essential from fish)
- omega-3 and omega-7 unsaturated fatty acids (where double bond is)
Na, K, Cl
important ions in membrane potentials and neural signal propagation
Ca
important in secretion neurotransmitters and regulatory functioning (don’t absorb in water)
Mg
important cofactor in several enzymes
carbohydrates
polysaccharides with alpha linakges
teeth
increase surface area accessible to digestive enzymes
- molars
- premolars
- canines
- incisors
milk teeth vs. permanent teeth
milk teeth fall out and are replaced by permanent
-some teeth grow continuously in some species
saliva
moisten food and start polysaccharide digestion using amylase
salivary glands
cells of salivary gland increase surface area and actively transport sodium chloride
-cells produce salivary anhydrase and bicarbonate that begins the break down of carbs
cardinal notch
where stomach and esophagus join
- no valve but thickening
- pyloric sphincter- opens periodically, end of stomach
regurgitation
- thickening at base of esophagus
- contract abdominal muscles
- flex neck so it goes out the mouth
digestive system
food processing and distribution with a unidirectional flow
-peristaltic movement in esophagus (contraction and relaxation)
stomach
release of acid and zymogens and increased motility stimulated by gastrin and smooth muscle contraction (auto stimulation)
end digestion: GIP and secretin (entergasterones that keep material in stomach)
enterogasterones
-blocks emptying of stomach (until processed)
-gastric inhibitory peptide (GIP) and secretin
(GIP and CCK also have role in ending feeding)
hormone gastrin
- polypeptide
- pyloric portion of stomach
- entry of food into stomach
- stimulates secretion of HCL and pepsinogen by stomach
cholecytokinin
- polypeptide
- fatty chyme in duodenum
- stimulates gall bladder contraction and secretion of digestive enzymes by pancreas
GIP
- polypeptide
- fatty chyme in duodenum
- inhibits stomach emptying
- stimulates insulin secretion (blood sugar level)
secretin
-polypeptide
-acidic chyme in duodenum
-stimulates secretion of bicarbonate by pancreas
(first hormone discovered)
start of digestion for small intestine
- arrival of chyme from stomach
- secretin releases basic juices and CCK, zymogen releases bile delivery
- duodenal enzyme entrokinase activates pancreatic zymogens
end digestion for small intestine
-somatostatin
VIP increases blood supply to gut
lacteal
extra return portion of circulatory system
-important role in absorbing fatty material
pancreas
-mixed function gland: exocrine for digestion and endocrine for glucose regulation release: ions/juices- secretin zymogens- CCK stopping secretins- enkephein
exocrine function of pancreas
-acinar cells secrete zymogens and pancreatic juices due to CCK and secretin