Energy Production and Metabolism — MCQs
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Mechanism of cyanide poisoning is by inhibiting: NEET 2013
NADH via glycerophosphate shunt makes how many ATP?
Fluoroacetate inhibits?
Which of the following processes does not occur in mitochondria?
Which enzyme catalyzes the rate limiting step in the TCA cycle?
Which of the following is not the source of cytosolic NADPH ?
Which enzyme is involved in substrate level phosphorylation?
Which enzyme primarily initiates the electron transport process in oxidative phosphorylation?
Anaplerotic reaction is catalyzed by?
Which of the following represents the most significant regulatory control point among these TCA cycle reactions?
Energy Production and Metabolism Indian Medical PG Practice Questions and MCQs
Question 311: Mechanism of cyanide poisoning is by inhibiting: NEET 2013
- A. DNA synthesis
- B. Cytochrome oxidase (Correct Answer)
- C. Protein breakdown
- D. Protein synthesis
Explanation: ***Cytochrome oxidase*** - **Cyanide** is a potent poison because it binds to the **ferric iron (Fe3+)** in the active site of **cytochrome c oxidase**. - This binding completely inhibits the enzyme, halting **cellular respiration** and **ATP production**, leading to rapid cell death. *DNA synthesis* - **Cyanide** does not directly inhibit **DNA polymerase** or other enzymes involved in DNA replication. - While overall cellular processes are disrupted, its primary toxic effect is not on DNA synthesis. *Protein breakdown* - **Cyanide** does not directly interfere with proteasomes or lysosomal enzymes responsible for **protein degradation**. - Its mechanism of action is upstream, affecting energy production necessary for all cellular processes, including protein turnover. *Protein synthesis* - **Cyanide** does not directly inhibit **ribosomes** or the enzymatic machinery for **protein synthesis**. - The lack of **ATP** caused by cyanide poisoning would eventually shut down protein synthesis, but this is a secondary effect, not the primary mechanism of action.
Question 312: NADH via glycerophosphate shunt makes how many ATP?
- A. 1
- B. 4
- C. 2 (Correct Answer)
- D. 3
Explanation: ***2*** - The **glycerol phosphate shuttle** transfers electrons from **cytosolic NADH** to **FAD** in the mitochondrial electron transport chain. - Each **FADH2** molecule produced then enters the electron transport chain at **Complex II**, ultimately leading to the generation of approximately **2 ATP** molecules. *1* - This option would be correct if the electrons were transferred to a molecule that yields only **one ATP** equivalent, which is not the case for **FADH2**. - No direct mechanism in a shunt generates exactly one ATP per NADH equivalent. *3* - This value represents the ATP yield from **NADH** when it directly enters the electron transport chain via the **malate-aspartate shuttle**, not the **glycerophosphate shuttle**. - The **glycerophosphate shuttle** is less efficient than the **malate-aspartate shuttle**. *4* - This number is not a standard ATP yield for either **NADH** or **FADH2** in the electron transport chain. - The maximum yield for NADH is typically considered to be 2.5 or 3 ATP, and for FADH2 is 1.5 or 2 ATP, depending on the shuttle and precise calculations.
Question 313: Fluoroacetate inhibits?
- A. Citrate synthase
- B. Succinate dehydrogenase
- C. Alpha-ketoglutarate dehydrogenase
- D. Aconitase (Correct Answer)
Explanation: ***Aconitase*** - **Fluoroacetate** is metabolically converted to **fluorocitrate**, which is a potent competitive inhibitor of **aconitase**. - **Aconitase** is the enzyme responsible for converting **citrate to isocitrate** in the **Krebs cycle**, and its inhibition blocks the cycle. *Citrate synthase* - This enzyme is responsible for the formation of **citrate** from **acetyl-CoA** and **oxaloacetate**. - While fluoroacetate indirectly affects the cycle, it does not directly inhibit **citrate synthase**. *Succinate dehydrogenase* - This enzyme is part of the **Krebs cycle** and the **electron transport chain**, converting **succinate to fumarate**. - **Malonate** is a competitive inhibitor of succinate dehydrogenase, not **fluoroacetate**. *Alpha-ketoglutarate dehydrogenase* - This enzyme catalyzes the conversion of **alpha-ketoglutarate to succinyl-CoA** in the **Krebs cycle**. - Specific inhibitors of this enzyme include **arsenite** and **mercury compounds**, but not fluoroacetate.
Question 314: Which of the following processes does not occur in mitochondria?
- A. Fatty acid oxidation
- B. Electron transport chain
- C. Glycogenolysis (Correct Answer)
- D. Citric acid cycle (Kreb's cycle)
Explanation: ***Glycogenolysis*** - **Glycogenolysis** is the breakdown of **glycogen** into glucose, which primarily occurs in the **cytosol** of cells, mainly in the liver and muscles. - This process is crucial for maintaining blood glucose levels and providing energy during periods of fasting or increased demand, and it does not take place within the mitochondria. *Fatty acid oxidation* - **Fatty acid oxidation**, also known as beta-oxidation, is a mitochondrial process that breaks down fatty acids into **acetyl-CoA** for energy production. - This occurs extensively within the mitochondrial matrix, producing ATP. *Electron transport chain* - The **electron transport chain** is located in the **inner mitochondrial membrane** and is the final stage of aerobic respiration, producing the majority of ATP. - It involves a series of protein complexes that transfer electrons to oxygen, creating a proton gradient for ATP synthesis. *Citric acid cycle (Kreb's cycle)* - The **citric acid cycle**, or **Krebs cycle**, is a central metabolic pathway that occurs in the **mitochondrial matrix**. - It oxidizes acetyl-CoA, derived from carbohydrates, fats, and proteins, to produce ATP, NADH, and FADH2.
Question 315: Which enzyme catalyzes the rate limiting step in the TCA cycle?
- A. Fumarase
- B. Aconitase
- C. Thiokinase
- D. α-ketoglutarate dehydrogenase (Correct Answer)
Explanation: **α-ketoglutarate dehydrogenase** - The **α-ketoglutarate dehydrogenase complex** catalyzes the oxidative decarboxylation of α-ketoglutarate to succinyl-CoA, producing NADH and CO2. - This step is a **major control point** in the TCA cycle and is highly regulated by: - **Product inhibition**: Succinyl-CoA and NADH - **Calcium ions**: Activate the enzyme - Along with isocitrate dehydrogenase and citrate synthase, it represents one of the three key regulatory enzymes of the TCA cycle. *Fumarase* - **Fumarase** catalyzes the reversible hydration of fumarate to L-malate. - This enzyme is **not a regulatory step** in the TCA cycle; its activity is typically high and not a control point for the overall flux of the cycle. *Aconitase* - **Aconitase** catalyzes the reversible isomerization of citrate to isocitrate, via the intermediate cis-aconitate. - While important for the cycle's progression, aconitase activity is **not considered a rate-limiting step** for the overall regulation of the TCA cycle. *Thiokinase* - The term **thiokinase** (or succinyl-CoA synthetase) catalyzes the reversible conversion of succinyl-CoA to succinate, coupled with GTP/ATP production. - This enzyme is responsible for **substrate-level phosphorylation** in the TCA cycle but does not represent a primary regulatory or rate-limiting step.
Question 316: Which of the following is not the source of cytosolic NADPH ?
- A. Malic enzyme
- B. G6PD
- C. Isocitrate dehydrogenase
- D. ATP citrate lyase (Correct Answer)
Explanation: ***ATP citrate lyase*** - **ATP citrate lyase** is an enzyme involved in the synthesis of **acetyl-CoA** from citrate in the cytosol, which is then used for **fatty acid synthesis**. It does not generate NADPH. - While the **acetyl-CoA** produced is used in pathways that require NADPH, ATP citrate lyase itself does not directly produce NADPH. *Isocitrate dehydrogenase* - Cytosolic **isocitrate dehydrogenase** catalyzes the oxidative decarboxylation of **isocitrate** to alpha-ketoglutarate, producing **NADPH**. - This reaction is an important source of **cytosolic NADPH**, especially in non-photosynthetic tissues. *Malic enzyme* - **Malic enzyme** catalyzes the oxidative decarboxylation of **malate** to pyruvate, simultaneously reducing **NADP+ to NADPH**. - This enzyme is a significant source of **cytosolic NADPH** in various tissues, contributing to fatty acid synthesis and other reductive processes. *G6PD* - **Glucose-6-phosphate dehydrogenase (G6PD)** is the rate-limiting enzyme in the **pentose phosphate pathway** (PPP). - It catalyzes the first step of the PPP, converting **glucose-6-phosphate** to 6-phosphogluconolactone and producing **NADPH** as a crucial coenzyme.
Question 317: Which enzyme is involved in substrate level phosphorylation?
- A. Enolase
- B. Aldolase
- C. Creatine kinase (Correct Answer)
- D. Lactate dehydrogenase
Explanation: ***Creatine kinase*** - **Creatine kinase** catalyzes the direct transfer of a high-energy phosphate group from **phosphocreatine** to **ADP** to form **ATP**. - This is a classic example of **substrate-level phosphorylation** - ATP formation by direct phosphate transfer from a high-energy donor molecule. - This reaction is crucial in muscle cells for rapid ATP regeneration during high-energy demand. - Other substrate-level phosphorylation enzymes include **phosphoglycerate kinase** and **pyruvate kinase** in glycolysis, and **succinyl-CoA synthetase** in the citric acid cycle. *Enolase* - **Enolase** converts **2-phosphoglycerate** to **phosphoenolpyruvate (PEP)** in glycolysis. - While this creates a high-energy phosphate compound, enolase itself does **not** catalyze substrate-level phosphorylation. - The actual ATP formation from PEP is catalyzed by **pyruvate kinase**, not enolase. *Aldolase* - **Aldolase** cleaves **fructose-1,6-bisphosphate** into **dihydroxyacetone phosphate** and **glyceraldehyde-3-phosphate**. - This is a cleavage reaction in glycolysis that does not involve ATP synthesis. *Lactate dehydrogenase* - **Lactate dehydrogenase** catalyzes the conversion of **pyruvate** to **lactate** with oxidation of **NADH to NAD+**. - This reaction regenerates NAD+ for glycolysis to continue but does not produce ATP.
Question 318: Which enzyme primarily initiates the electron transport process in oxidative phosphorylation?
- A. Pyruvate kinase
- B. Succinyl CoA thiokinase
- C. NADH dehydrogenase (Correct Answer)
- D. ATP synthase
Explanation: ***Correct NADH dehydrogenase*** - **NADH dehydrogenase**, also known as Complex I, is the enzyme that accepts electrons from **NADH** during oxidative phosphorylation, initiating the electron transport chain. - This enzyme **oxidizes NADH** to NAD+ and pumps protons from the mitochondrial matrix to the intermembrane space, contributing to the **proton gradient**. *Incorrect Pyruvate kinase* - **Pyruvate kinase** is an enzyme involved in **glycolysis**, catalyzing the final step of converting phosphoenolpyruvate to pyruvate. - It functions in the **cytoplasm** and is not directly involved in the electron transport chain or oxidative phosphorylation. *Incorrect Succinyl CoA thiokinase* - **Succinyl CoA thiokinase** (also known as succinate thiokinase or succinyl-CoA synthetase) is an enzyme in the **Krebs cycle** (citric acid cycle). - It catalyzes the reversible reaction of converting succinyl-CoA to succinate and is not directly part of the electron transport chain. *Incorrect ATP synthase* - **ATP synthase** (Complex V) is the enzyme responsible for synthesizing ATP using the **proton gradient** established by the electron transport chain. - While crucial for oxidative phosphorylation, it acts at the end of the process, utilizing the energy generated, rather than initiating electron transport.
Question 319: Anaplerotic reaction is catalyzed by?
- A. Enolase
- B. Pyruvate kinase
- C. G6PD
- D. Pyruvate carboxylase (Correct Answer)
Explanation: ***Pyruvate carboxylase*** - **Pyruvate carboxylase** catalyzes the ATP-dependent carboxylation of **pyruvate** to **oxaloacetate**. - This reaction is crucial for replenishing intermediates of the **citric acid cycle**, making it an anaplerotic reaction. *Enolase* - **Enolase** catalyzes the conversion of **2-phosphoglycerate** to **phosphoenolpyruvate** in **glycolysis**. - This reaction is part of catabolism and does not replenish citric acid cycle intermediates. *Pyruvate kinase* - **Pyruvate kinase** catalyzes the final step of **glycolysis**, converting **phosphoenolpyruvate** to **pyruvate**. - This enzyme is involved in ATP production and the overall catabolic pathway of glucose. *G6PD* - **Glucose-6-phosphate dehydrogenase (G6PD)** is the rate-limiting enzyme in the **pentose phosphate pathway**. - It produces **NADPH** and precursors for nucleotide synthesis, but not directly involved in anaplerotic reactions for the citric acid cycle.
Question 320: Which of the following represents the most significant regulatory control point among these TCA cycle reactions?
- A. Succinyl-CoA to Succinate (Succinyl-CoA synthetase)
- B. Isocitrate to Alpha-ketoglutarate (Isocitrate dehydrogenase) (Correct Answer)
- C. Acetyl-CoA + Oxaloacetate to Citrate (Citrate synthase)
- D. Alpha-ketoglutarate to Succinyl-CoA (Alpha-ketoglutarate dehydrogenase complex)
Explanation: ***Isocitrate to Alpha-ketoglutarate (Isocitrate dehydrogenase)*** - **Isocitrate dehydrogenase** is the **rate-limiting enzyme** and the **most significant regulatory control point** of the TCA cycle - It catalyzes the first **irreversible NADH-generating step** after citrate formation, making it the key determinant of cycle flux - Strongly **activated by ADP** (indicating low energy status) and **Ca²⁺** (in mitochondria) - Strongly **inhibited by NADH and ATP** (indicating high energy status), providing sensitive energy-status regulation - This is the primary control point recognized in standard biochemistry references *Alpha-ketoglutarate to Succinyl-CoA (Alpha-ketoglutarate dehydrogenase complex)* - The **alpha-ketoglutarate dehydrogenase complex** is an important regulatory enzyme with irreversible catalysis - Inhibited by its products **NADH** and **succinyl-CoA**, as well as by **ATP** - While it is one of the three main control points, it is considered a **secondary regulatory site** compared to isocitrate dehydrogenase *Acetyl-CoA + Oxaloacetate to Citrate (Citrate synthase)* - **Citrate synthase** catalyzes the first committed step of the TCA cycle and is the entry point for acetyl-CoA - Subject to **product inhibition by citrate** and allosteric inhibition by **ATP, NADH, and succinyl-CoA** - Although highly regulated and crucial for initiating the cycle, it is not the rate-limiting step *Succinyl-CoA to Succinate (Succinyl-CoA synthetase)* - This reaction involves **substrate-level phosphorylation** to produce **GTP (or ATP)** - It is a **reversible reaction** and generally not a primary regulatory step - Regulation depends mainly on substrate availability rather than complex allosteric control mechanisms
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