What does a high NADH/NAD+ ratio indicate?
A. Increased oxidation capacity
B. Increased need for ATP production
C. High energy status, slowing TCA cycle
D. Activation of dehydrogenases
C. High energy status, slowing TCA cycle
What is the net ATP yield in the complete oxidation of 1mole of glucose to CO2 and water in the liver?
A. 10
B. 20
C. 30
D. 32
D. 32
How many ATPs are synthesized in the muscles via glycolysis, PDH and TCA cycle?
30
Only 30 because glycolysis lacks 2 ATP dt usage of FADH not NADH
Which step of the TCA cycle produces GTP by substrate-level phosphorylation?
A. Isocitrate → α-ketoglutarate
B. α-Ketoglutarate → Succinyl-CoA
C. Succinyl-CoA → Succinate
D. Malate → Oxaloacetate
C. Succinyl-CoA → Succinate
If you were to design a drug to slow down the TCA cycle for cancer therapy, which enzyme would be the best target?
A. Succinate thiokinase
B. Malate dehydrogenase
C. Isocitrate dehydrogenase
D. Fumarase
C. Isocitrate dehydrogenase
Which enzyme of the TCA cycle is also part of the electron transport chain (Complex II)?
A. Citrate synthase
B. Succinate dehydrogenase
C. Aconitase
D. Malate dehydrogenase
B. Succinate dehydrogenase
Why does inhibition of aconitase by fluorocitrate cause citrate to accumulate?
A. Citrate synthase activity increases
B. Citrate cannot be isomerized to isocitrate
C. Succinate dehydrogenase is inhibited
D. NADH levels rise, blocking citrate breakdown
B. Citrate cannot be isomerized to isocitrate
Which cofactor is NOT required by the α-ketoglutarate dehydrogenase complex?
A. Thiamine pyrophosphate (TPP)
B. Lipoic acid
C. FAD
D. Biotin
D. Biotin
A patient with thiamine deficiency will have impaired activity of which TCA enzyme?
A. Succinate dehydrogenase
B. Isocitrate dehydrogenase
C. α-Ketoglutarate dehydrogenase
D. Malate dehydrogenase
C. α-Ketoglutarate dehydrogenase
Why is the Citric Acid Cycle considered amphibolic?
A. produces only energy
B. helps synthesize ATP only during fasting
C. functions in both breakdown & synthesis of molecules
D. requires only acetyl-CoA as input
C. functions in both breakdown & synthesis of molecules
Why does high NADH/NAD⁺ ratio inhibit PDH activity?
A. It increases CoA availability
B. It signals high energy status, activating PDH kinase
C. It enhances Ca²⁺ binding to PDH phosphatase
D. It promotes thiamine pyrophosphate formation
B. It signals high energy status, activating PDH kinase
Increase in energy stops production
Which of the following best explains why arsenic poisoning inhibits PDC activity?
A. Arsenic binds irreversibly to the FAD-binding site in E3
B. Arsenic binds to sulfhydryl groups in lipoic acid, preventing acetyl transfer
C. Arsenic competes with NAD⁺ for binding to E3
D. Arsenic directly decarboxylates pyruvate, bypassing PDC
B. Arsenic binds to sulfhydryl groups in lipoic acid, preventing acetyl transfer
Arsenide has a high affinity to sulfhydryl groups
A patient presents with neurological symptoms due to a thiamine deficiency. Which step of the PDC function will be directly impaired?
A. Acetyl group transfer from lipoic acid to CoA
B. Oxidation of dihydrolipoamide by FAD
C. Decarboxylation of pyruvate
D. Electron transfer from NADH to the ETC
C. Decarboxylation of pyruvate
Which cofactor is bound to the E1 subunit of the pyruvate dehydrogenase complex?
A. Lipoic acid
B. FAD
C. Thiamine pyrophosphate (TPP)
D. Coenzyme A
C. Thiamine pyrophosphate (TPP)
Which of the following statements is TRUE of PDH reaction?
A. It produces glucose from pyruvate
B. It converts acetyl-CoA into pyruvate
C. It converts pyruvate into acetyl-CoA
D. It regenerates NAD⁺ for glycolysis
C. It converts pyruvate into acetyl-CoA
Which enzyme in the PDH complex is responsible for the decarboxylation of pyruvate?
a) Dihydrolipoyl transacetylase (E2)
b) Pyruvate dehydrogenase (E1)
c) Dihydrolipoyl dehydrogenase (E3)
d) Citrate synthase
b) Pyruvate dehydrogenase (E1)
What is the coenzyme required by the Pyruvate dehydrogenase (E1) enzyme for decarboxylation?
a) Lipoic acid
b) Coenzyme A
c) Thiamine pyrophosphate (TPP)
d) NAD+
c) Thiamine pyrophosphate (TPP)
In the PDH complex, what is the direct carrier of the two-carbon acetyl group before it is transferred to Coenzyme A?
a) Oxidized lipoamide
b) Acetyl lipoamide
c) Hydroxyethyl TPP
d) NADH
b) Acetyl lipoamide
What cofactor is required for the regeneration of oxidized lipoamide by dihydrolipoyl dehydrogenase (E3)?
a) NAD+ and FAD
b) TPP and CoA
c) ATP and ADP
d) NADH and FADH2
a) NAD+ and FAD
Which molecule is the final product of the PDH complex that enters the TCA cycle?
a) Pyruvate
b) Acetyl-CoA
c) Citrate
d) Succinyl-CoA
b) Acetyl-CoA
What are the five cofactors of the PDH complex?
a) ATP, NADH, FAD, CoA, Biotin
b) TPP, Lipoic acid, CoA, FAD, NAD+
c) NAD+, FAD, Biotin, ATP, CoA
d) TPP, CoA, ATP, NADH, Lipoic acid
b) TPP, Lipoic acid, CoA, FAD, NAD+
Which step of the PDH complex reaction produces CO2?
a) Transfer of acetyl group to CoA
b) Reoxidation of lipoamide
c) Decarboxylation of pyruvate to hydroxyethyl TPP
d) Conversion of NAD+ to NADH
c) Decarboxylation of pyruvate to hydroxyethyl TPP
How is the PDH complex regulated by phosphorylation?
a) Phosphorylation activates PDH complex
b) Phosphorylation inhibits PDH complex by PDH kinase
c) Dephosphorylation inhibits PDH complex
d) It is not regulated by phosphorylation
b) Phosphorylation inhibits PDH complex by PDH kinase
What allosteric effectors activate PDH kinase leading to PDH complex inhibition?
a) ADP and pyruvate
b) Acetyl-CoA, NADH, and ATP
c) Calcium ions
d) Insulin and catecholamines
b) Acetyl-CoA, NADH, and ATP