What is the net number of ATP molecules and NADH formed in glycolysis per glucose molecule?
Which enzyme primarily initiates the electron transport process in oxidative phosphorylation?
In the electron transport chain (ETC), which enzyme does cyanide inhibit?
NADH via glycerophosphate shunt makes how many ATP?
What is the role of nonsense codons in protein synthesis?
Which hormone is known to repress the biosynthesis of the enzyme pyruvate carboxylase?
Which molecule serves as a key link between carbohydrate metabolism and fatty acid synthesis?
Which carbohydrate is primarily metabolized by Aldolase-B?
Which vitamin is involved in one-carbon transfer reactions?
What is the cofactor required for the enzyme xanthine oxidase?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 31: What is the net number of ATP molecules and NADH formed in glycolysis per glucose molecule?
- A. 4 ATP, 2 NADH
- B. 4 ATP, 4 NADH
- C. 2 ATP, 4 NADH
- D. 2 ATP, 2 NADH (Correct Answer)
Explanation: **2 ATP, 2 NADH** - Glycolysis has a net yield of **2 molecules of ATP** because 4 ATP molecules are produced, but 2 ATP molecules are consumed during the initial energy investment phase. - **2 molecules of NADH** are also produced during the energy generation phase when glyceraldehyde-3-phosphate is oxidized. *4 ATP, 2 NADH* - While 4 ATP molecules are indeed produced during glycolysis, this option does not account for the **2 ATP molecules consumed** in the initial steps, leading to an incorrect net value. - The production of **2 NADH** is correct, but the ATP count is the gross rather than the net. *4 ATP, 4 NADH* - This option overstates the production of both ATP and NADH. While **4 ATP are produced (gross)**, the net is 2 ATP. - Only **2 NADH** molecules are formed per glucose molecule in glycolysis, not 4. *2 ATP, 4 NADH* - This option accurately reflects the **net ATP yield of 2 molecules**. - However, it exaggerates the production of NADH, as only **2 molecules of NADH** are formed during glycolysis, not 4.
Question 32: 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 33: In the electron transport chain (ETC), which enzyme does cyanide inhibit?
- A. Complex II (Succinate dehydrogenase)
- B. Cytochrome c oxidase (Complex IV) (Correct Answer)
- C. Complex I (NADH dehydrogenase)
- D. Complex III (Cytochrome bc1 complex)
Explanation: ***Cytochrome c oxidase (Complex IV)*** - Cyanide binds to the **ferric iron (Fe3+)** in the heme a3 component of cytochrome c oxidase, blocking the final transfer of electrons to oxygen. - This inhibition effectively halts the entire **electron transport chain** and **oxidative phosphorylation**, leading to rapid cellular energy depletion. *Complex I (NADH dehydrogenase)* - While other toxins can inhibit Complex I (e.g., rotenone, amytal), **cyanide specifically targets Complex IV**. - Inhibition here prevents the entry of electrons from **NADH** into the ETC, but it's not cyanide's primary site of action. *Complex III (Cytochrome bc1 complex)* - Complex III is involved in transferring electrons from **ubiquinol** to cytochrome c, but it is not directly inhibited by cyanide. - Antimycin A is a well-known inhibitor of Complex III. *Complex II (Succinate dehydrogenase)* - Complex II directly receives electrons from **succinate** in the citric acid cycle and passes them to ubiquinone, bypassing Complex I. - Cyanide does not inhibit Complex II; inhibitors of this complex include malonate.
Question 34: 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 35: What is the role of nonsense codons in protein synthesis?
- A. Elongation of the polypeptide chain
- B. Pre-translational modification of proteins
- C. Initiation of protein synthesis
- D. Termination of protein synthesis (Correct Answer)
Explanation: ***Termination of protein synthesis*** - **Nonsense codons**, also known as **stop codons** (UAA, UAG, UGA), signal the end of translation. - When a ribosome encounters a nonsense codon, it binds **release factors** instead of an aminoacyl-tRNA, leading to the dissociation of the polypeptide chain. *Elongation of the polypeptide chain* - **Elongation** involves the sequential addition of amino acids to the growing polypeptide chain, guided by sense codons. - Nonsense codons do not code for any amino acid and thus do not contribute to chain elongation. *Pre-translational modification of proteins* - **Pre-translational modifications** refer to events like protein folding and disulfide bond formation that occur as the polypeptide is being synthesized. - Nonsense codons are involved in halting the synthesis, not in modifying the protein. *Initiation of protein synthesis* - **Initiation** of protein synthesis begins at the **start codon** (AUG), which codes for methionine. - Nonsense codons are distinct from the start codon and fulfill a different role in the translation process.
Question 36: Which hormone is known to repress the biosynthesis of the enzyme pyruvate carboxylase?
- A. Cortisol
- B. Glucagon
- C. Insulin (Correct Answer)
- D. Growth hormone
Explanation: ***Insulin*** - **Insulin** is an anabolic hormone that promotes glucose utilization and opposes **gluconeogenesis**. - While insulin does inhibit hepatic glucose production, it primarily acts by **repressing PEPCK (phosphoenolpyruvate carboxykinase)**, the rate-limiting enzyme of gluconeogenesis, rather than directly repressing pyruvate carboxylase biosynthesis. - **Note:** Modern biochemistry emphasizes that insulin's main transcriptional target in gluconeogenesis is **PEPCK**, not pyruvate carboxylase. However, this was the expected answer for **NEET-2012**, reflecting the understanding at that time. - Insulin also promotes dephosphorylation and inactivation of gluconeogenic enzymes and enhances glucose uptake and glycolysis. *Glucagon* - **Glucagon** is a catabolic hormone that **activates** enzymes involved in **gluconeogenesis** and glycogenolysis to raise blood glucose levels. - It would **increase**, not repress, the biosynthesis and activity of gluconeogenic enzymes including **pyruvate carboxylase**. *Cortisol* - **Cortisol** is a glucocorticoid hormone that **stimulates gluconeogenesis** in the liver as part of the stress response. - It typically **upregulates** the synthesis and activity of gluconeogenic enzymes like **pyruvate carboxylase** and **PEPCK**. *Growth hormone* - **Growth hormone** generally **increases insulin resistance** and can have a **diabetogenic effect**, promoting glucose production rather than repressing gluconeogenic enzymes. - It does not directly repress gluconeogenic enzyme biosynthesis; its metabolic effects favor lipolysis and protein synthesis.
Question 37: Which molecule serves as a key link between carbohydrate metabolism and fatty acid synthesis?
- A. Glucose-6-phosphate
- B. Acetyl-CoA
- C. Citrate (Correct Answer)
- D. Succinyl-CoA
Explanation: ***Citrate*** - **Citrate** is the crucial molecule that links carbohydrate metabolism to fatty acid synthesis via the **citrate-malate shuttle** - In the fed state, excess **acetyl-CoA** (derived from glucose metabolism via glycolysis and pyruvate dehydrogenase) condenses with oxaloacetate to form citrate in the mitochondria - **Citrate** is then transported from mitochondria to the cytosol, where **ATP-citrate lyase** cleaves it to regenerate **acetyl-CoA** and **oxaloacetate** for fatty acid synthesis - This is the primary mechanism for transporting acetyl-CoA equivalents from mitochondria (where glucose is oxidized) to the cytosol (where fatty acids are synthesized) - Citrate also acts as an **allosteric activator** of **acetyl-CoA carboxylase**, the rate-limiting enzyme of fatty acid synthesis *Glucose-6-phosphate* - While **glucose-6-phosphate** is a key intermediate in glycolysis and gluconeogenesis, it is not the molecule that directly links carbohydrate breakdown to fatty acid synthesis - It is several steps removed from the generation of cytosolic acetyl-CoA needed for fatty acid synthesis *Acetyl-CoA* - **Acetyl-CoA** is the direct precursor for fatty acid synthesis - However, acetyl-CoA generated in mitochondria from glucose oxidation **cannot directly cross the mitochondrial membrane** - It must be transported as citrate, making citrate the actual linking molecule between the two compartments *Succinyl-CoA* - **Succinyl-CoA** is a Krebs cycle intermediate involved in heme synthesis and propionate metabolism - It is not involved in transporting acetyl units from mitochondria to cytosol for fatty acid synthesis
Question 38: Which carbohydrate is primarily metabolized by Aldolase-B?
- A. Galactose
- B. Fructose (Correct Answer)
- C. Sucrose
- D. None of the options
Explanation: ***Fructose*** - **Aldolase B** is a key enzyme in the liver responsible for the metabolism of **fructose**, specifically cleaving **fructose-1-phosphate** into **dihydroxyacetone phosphate** and **glyceraldehyde**. - A deficiency in **Aldolase B** leads to **hereditary fructose intolerance**, causing an accumulation of **fructose-1-phosphate** after fructose ingestion. *Galactose* - **Galactose** is primarily metabolized by enzymes in the **Leloir pathway**, including **galactokinase** and **galactose-1-phosphate uridylyltransferase**. - **Aldolase B** plays no significant role in the metabolism of galactose. *Sucrose* - **Sucrose** is a disaccharide composed of **glucose** and **fructose**. - It is first broken down by **sucrase** in the small intestine into its constituent monosaccharides before they are metabolized further. *None of the options* - This option is incorrect because **fructose** is indeed a carbohydrate primarily metabolized by Aldolase-B. - The enzyme's specific role in fructose metabolism is well-established.
Question 39: Which vitamin is involved in one-carbon transfer reactions?
- A. Folic acid (Correct Answer)
- B. Pantothenic acid
- C. Niacin
- D. Thiamine
Explanation: ***Folic acid*** - **Folic acid (Vitamin B9)** is a crucial coenzyme in the form of **tetrahydrofolate (THF)**, which acts as a carrier of **one-carbon units**. - These one-carbon units are essential for various metabolic pathways, including the synthesis of **purines**, **thymidylate**, and the metabolism of several **amino acids**. *Pantothenic acid* - **Pantothenic acid (Vitamin B5)** is a precursor to **Coenzyme A (CoA)**, which plays a central role in fatty acid metabolism and the **Krebs cycle**, not one-carbon transfers. - CoA is involved in transferring **acetyl groups**, not one-carbon units. *Niacin* - **Niacin (Vitamin B3)** is a component of **NAD+** and **NADP+**, which are vital coenzymes in **redox reactions** (electron transfer), not one-carbon metabolism. - It functions primarily in **energy metabolism** as an electron carrier. *Thiamine* - **Thiamine (Vitamin B1)** is a coenzyme for **dehydrogenase reactions** and **transketolase** in the **pentose phosphate pathway**, which are involved in carbohydrate metabolism. - It does not directly participate in one-carbon transfer reactions.
Question 40: What is the cofactor required for the enzyme xanthine oxidase?
- A. Selenium
- B. Zinc
- C. Molybdenum (Correct Answer)
- D. Magnesium
Explanation: ***Molybdenum*** - **Xanthine oxidase** is a key enzyme in **purine metabolism**, responsible for the oxidation of **hypoxanthine to xanthine** and further to **uric acid**. - **Molybdenum** is an essential trace element that serves as a **cofactor** for several enzymes, including xanthine oxidase, where it helps facilitate electron transfer reactions. *Selenium* - **Selenium** is a cofactor for **glutathione peroxidase**, an enzyme involved in antioxidant defense. - It is not directly involved in the function of **xanthine oxidase**. *Zinc* - **Zinc** is a cofactor for a wide range of enzymes, including **carbonic anhydrase** and **alcohol dehydrogenase**. - It does not serve as a cofactor for **xanthine oxidase**. *Magnesium* - **Magnesium** is a critical cofactor for many enzymes, particularly those involved in **ATP hydrolysis and synthesis** and **DNA/RNA synthesis**. - It is not a cofactor for **xanthine oxidase**.