Biochem Exam 3

Bonds oxidized for energy production

CC and CH

Oxidation reactions in metabolism

not direct with O2

delta G

negative is exergonic/reactants to product/favorable, positive is endergonic/products to reactants

delta H

negative is exothermic/releases heat/favorable, positive is endothermic/heat input

delta S

negative is decrease in entropy, postive is increase in entropy and is favorable

ATP

universal energy carrier, kinetically stable, little non-enzymatic breakdown

Glycolysis step 1

hexokinase reaction, glucose phosphorylation coupled to ATP breakdown

Glycolysis step 2

phosphohexase isomerase, rearrange C=O

Glycolysis step 3

PFK-1, activated by high ADP or AMP, break down ATP, irreversible

Glycolysis step 4

aldolase, hexose into 2 trioses 

Glycolysis step 5

triose phosphate isomerase (TPI)

Glycolysis step 6

oxidation of G3P, dehydrogenase reaction, only redox reaction, reduction of NAD+

Glycolysis step 7

phosphoglucerate kinase, first payoff coupled to substrate level phosphorylation 

Glycolysis step 8

phosphate mutase, isomerization reaction

Glycolysis step 9

formation of phosphoenolpyruvate by enolase, dehydration reaction 

Glycolysis step 10

ATP from PEP, second payoff

Prepatory stage

C6 into 2 C3

Payoff stage

2 C3 into 2 pyruvate

Coupling a reaction to ATP breakdown

can make an unfavorable reaction favorable

Fermentation

anaerobic, pyruvate into lactate or ethanol

Citric acid cycle

aerobic, acetyl CoA into CO2 and H2O

NAD+ regeneration in fermentation

restored from NADH by lactate dehydrogenase or alcohol dehydrogenase

E1 subunit (pyruvate DH)

decarboxylation, kicks off CO2

E2 subunit (pyruvate DH)

oxidation, acetyl CoA leaves, reduced lipoic acid 

E3 subunit (pyruvate DH)

shutling electrons to a NAD+ carrier, enables PDH to go another round, transferred through FAD

PDH inhibited by

NADH, ATP, acetyl CoA

PDH activated by

NAD+, AMP, CoA

PDH cofactors

thiamine pyrophosphate, lipoate, NAD+, FAD, CoA

CAC step 1

citrate synthase joins acetyl CoA and oxaloacetate to form citrate, condensation reaction

CAC step 2

aconitase isomerizes citrate into isocitrate, isomerization

CAC step 3

isocitrate dehydrogenase oxidizes isocitrate producing a-ketoglutarate, oxidative decarboxylation, NAD+ reduced, CO2 released 

CAC step 4

a-ketodehydrogenase oxidizes a-keto producing succinyl-CoA, oxidative decarboxylation, NAD+ reduced, CO2 released 

CAC step 5

succinyl-CoA synthetase harvests energy of thiodester, subtraste level phosphorylation, GTP produced 

CAC step 6

succinate dehydrogenase, dehydrogenation, FAD to FADH2

CAC step 7

fumarase hydrates fumarase into L-malase, hydration, FAD to FADH2

CAC step 8

malate dehydrogenase, dehydrogenation

CAC location

mitochondria

A-ketodehydrogenase vs PDH

same cofactors, similar E1 and E2, identical E3

Why fats are preferred long term energy storage molecule

twice the amount of calories per gram, can get more energy out of them 

Fatty acid activation

joined to CoA, activated by acetyl CoA synthetases on outer mitochondrial membrane

Fatty acids entering mitochondria

transport across inner mitochondrial membrane into matrix by carnitine carrier system 

B-oxidation step 1

dehydrogenation, lose H, FAD into FADH2

B-oxidation step 2

hydration

B-oxidation step 3

dehydrogenation, oxidation of B-C bond, NAD into NADH

B-oxidation step 4

thiolytic clevage, catalyzed by thiolase, CC to CH

Rounds of B-oxidation per fatty acid carbon number

carbons divided by 2 equal number of acetyl-CoAs, subtract 1 equals rounds

NADH and FADH2 number per carbon number

equal to acetyl CoAs minus 1 

Franz Knoop’s findings

B-oxidation happens in stepwise breakdownof 2C units

Amino acid catabolism

more complicated

Aminotransferases

catalyze removal of amino groups in keto acids via transaminations, involve glutamate and a-ketoglutarate

2 nitrogens for urea

1 from NH4, 1 from aspartate

NH4 entering urea cycle

joined to CO2 to form carbamoyl phosphate

NH4 leaving urea cycle

urea is released by arginase and exits the cytosol

Glucogenic

can be turned into glucose

Ketogenic

can’t be turned into glucose

Orinthine transcarbamylase deficiency

increased orinthine, carbamoyl phosphate, and ammonia, decrease in citriline and urea 

Higher E’

higher affinity for electrons, goes in forward direction, reduced

Lower E’

lower affinity for electrons, backwards direction, oxidized 

Complex 1 (ETC)

catalyzes oxidation of NADH and reduction of UQ, pumps 4H+

Complex 2 (ETC)

catalyzes oxidation of succinate into fumurate, reduction of UQ

Complex 3 (ETC)

oxidizes ubiquinol and reduces Cyt C1, pumps 4H+ per 2e-, Cyt c shuttles electrons 

Complex 4 (ETC)

O2 consumed by respiring organs, pumps 2H+ per 2e-, reduces O2 to 2 H2O

Proton-motive force

gradient of H+ that contributes to chemical potential energy and electrical potential

How ATP can be made

substrate level phosphorylation and chemiosmosis

DNP

uncouples reaction, causes O2 consumption without ATP synthesis 

Thermogenin

uncoupler, electron transport happens with less energy conserved in ATP, burn more fat and produce more heat and water 

a and B subunits (ATP synthase)

work together to bind ADP and Pi

Y subunit (ATP synthase)

causes rotation to cycle ATPs

C subunit (ATP synthase)

bind to protons, 12 subunits

Stoichiometry of ATP synthase

12 C subunits, 12 H+ per 3 ATP

Proton gradient affect on pH

mitochondrial matrix is 1 pH unit higher than intermembrane space when active, 10x difference in amount of protons