Energy Production and Metabolism — MCQs

Energy Production and Metabolism Indian Medical PG Practice Questions and MCQs

Question 291: Which of the following is not a free radical?

A. Superoxide anion
B. Hydrogen peroxide (H2O2) (Correct Answer)
C. Nitric oxide (NO·)
D. Hydroxyl radical (.OH)

Explanation: ***Hydrogen peroxide (H₂O₂)*** - **Hydrogen peroxide** is a **reactive oxygen species (ROS)** but is not a free radical because it has **no unpaired electrons** in its outermost shell. - While it can be converted into the highly reactive hydroxyl radical via the **Fenton reaction**, it is stable enough to be transported across membranes. *Superoxide anion (O₂⁻)* - The **superoxide anion (O₂⁻)** is a free radical because it has an **unpaired electron** in its outer shell. - It is one of the primary **reactive oxygen species** formed during cellular metabolism and can damage cellular components. *Nitric oxide (NO·)* - **Nitric oxide** is an important **free radical** with a single **unpaired electron** in its molecular structure. - It functions as a vital signaling molecule in vascular biology, regulating blood pressure and neurotransmission, despite being a free radical. *Hydroxyl radical (·OH)* - The **hydroxyl radical (·OH)** is one of the most reactive and damaging **free radicals** in biological systems. - It has a single **unpaired electron**, making it highly unstable and able to react indiscriminately with virtually all types of biomolecules.

Question 292: Pyruvate dehydrogenase requires all cofactors except:

A. Thiamin
B. Pyridoxin (Vitamin B6) (Correct Answer)
C. Riboflavin
D. Niacin

Explanation: ***Pyridoxin (Vitamin B6)*** - **Pyridoxin** (vitamin B6) is a coenzyme for many enzymes involved in **amino acid metabolism**, but it is **not directly required** by the pyruvate dehydrogenase complex. - The pyruvate dehydrogenase complex uses **thiamine pyrophosphate**, **lipoic acid**, **FAD**, **NAD+**, and **Coenzyme A** as cofactors. *Thiamin* - **Thiamin pyrophosphate** (TPP), derived from thiamin (vitamin B1), is a crucial coenzyme for the **E1 subunit** of the pyruvate dehydrogenase complex. - It participates in the **decarboxylation** of pyruvate, releasing CO2. *Riboflavin* - **FAD** (flavin adenine dinucleotide), derived from riboflavin (vitamin B2), is a coenzyme for the **E3 subunit** (dihydrolipoyl dehydrogenase) of the pyruvate dehydrogenase complex. - It is involved in the **regeneration of oxidized lipoamide**. *Niacin* - **NAD+** (nicotinamide adenine dinucleotide), derived from niacin (vitamin B3), is a coenzyme for the **E3 subunit** of the pyruvate dehydrogenase complex. - It acts as an **electron acceptor** during the reoxidation of FADH2.

Question 293: In the malate shuttle, how many ATPs are produced from one NADH?

A. 1 ATP
B. 3 ATP
C. 2 ATP
D. 2.5 ATP (Correct Answer)

Explanation: ***2.5 ATP*** - In the **malate-aspartate shuttle**, mitochondrial **NADH** is regenerated from cytosolic NADH, and then enters the electron transport chain at **Complex I**. - **Complex I** entry means that NADH contributes to the pumping of enough protons to generate approximately **2.5 ATP** through oxidative phosphorylation. *1 ATP* - **1 ATP** is not the direct equivalent produced from the reoxidation of one NADH via the malate shuttle into the electron transport chain. - This value is typically associated with the direct hydrolysis of **ATP** or the energy equivalent of **GTP** produced in the citric acid cycle. *3 ATP* - Historically, **3 ATP** was the accepted stoichiometry for one NADH, but more accurate measurements of proton pumping and ATP synthase activity have revised this. - The value of 3 ATP per NADH does not reflect the most current understanding of mitochondrial bioenergetics. *2 ATP* - **2 ATP** is the approximate yield for **FADH2** entering the electron transport chain at **Complex II**, bypassing Complex I, and thus pumping fewer protons. - This value is not applicable to NADH transferred via the malate-aspartate shuttle, as NADH enters at Complex I.

Question 294: Energy source used by brain in later days of starvation is

A. Glucose
B. Ketone bodies (Correct Answer)
C. Glycogen
D. Fatty acids

Explanation: ***Ketone bodies*** - During **prolonged starvation**, the liver produces **ketone bodies** (acetoacetate and β-hydroxybutyrate) from fatty acid breakdown. - The brain adapts to utilize these ketone bodies as a primary energy source, reducing its reliance on **glucose**. *Glucose* - While **glucose** is the primary energy source for the brain under normal conditions, its availability diminishes significantly during prolonged starvation. - The brain attempts to conserve glucose for essential functions by switching to alternative fuels. *Glycogen* - The brain stores very limited amounts of **glycogen**, which are rapidly depleted within minutes of glucose deprivation. - It is not a sustainable or significant energy source during extended periods of starvation. *Fatty acids* - **Fatty acids** cannot directly cross the **blood-brain barrier** to a significant extent, thus they are not a direct fuel source for brain cells. - They are, however, used by the liver to synthesize ketone bodies, which then serve as brain fuel.

Question 295: Which metabolic pathway is least active during 12 days of fasting?

A. Gluconeogenesis
B. Glycogenolysis (Correct Answer)
C. Ketogenesis
D. Lipolysis

Explanation: ***Correct: Glycogenolysis*** - **Glycogenolysis**, the breakdown of glycogen stores, is very active during the **initial hours of fasting** (first 24-48 hours) to maintain blood glucose levels. - However, after **12 days of fasting**, liver and muscle **glycogen stores are completely depleted**, making this pathway **essentially inactive** or the least active of all the metabolic pathways. - Once glycogen is exhausted, this pathway cannot contribute further to energy metabolism. *Incorrect: Gluconeogenesis* - This pathway becomes **increasingly active** during prolonged fasting to **synthesize new glucose** from non-carbohydrate precursors (amino acids, lactate, glycerol). - Essential for maintaining blood glucose for **glucose-dependent tissues** like red blood cells and parts of the brain that haven't fully adapted to ketones. - Remains a **crucial and active pathway** throughout prolonged fasting. *Incorrect: Ketogenesis* - **Ketogenesis** is **highly active** during prolonged fasting, producing **ketone bodies** (acetoacetate, β-hydroxybutyrate) from fatty acids in the liver. - Provides the **primary alternative fuel** for the brain (up to 70% of brain energy needs) and other tissues. - This is a **key metabolic adaptation** to preserve protein and glucose during starvation. *Incorrect: Lipolysis* - **Lipolysis** (breakdown of triglycerides into fatty acids and glycerol) is **highly active** during fasting to mobilize stored energy. - Provides **fatty acids** for direct oxidation by most tissues and **glycerol** as a gluconeogenic substrate. - A **fundamental process** for energy supply during nutrient deprivation.

Question 296: Chemical process involved in conversion of progesterone to glucocorticoids is

A. Methylation
B. Hydroxylation (Correct Answer)
C. Carboxylation
D. None of the options

Explanation: ***Hydroxylation*** - The conversion of progesterone to glucocorticoids involves several enzymatic steps, with **hydroxylation reactions** being critical for adding hydroxyl groups at specific carbon positions (e.g., C-17, C-21, C-11). - These hydroxylation steps are catalyzed by various **cytochrome P450 enzymes** (e.g., 17α-hydroxylase, 21-hydroxylase, 11β-hydroxylase) within the adrenal cortex, leading to the formation of active glucocorticoids like **cortisol**. *Methylation* - **Methylation** involves the addition of a methyl group (-CH₃) to a molecule, a process more commonly associated with modifying DNA, proteins, or certain neurotransmitters. - While methylation is a vital biological process, it is not the primary chemical reaction involved in the **steroidogenesis pathway** converting progesterone to glucocorticoids. *Carboxylation* - **Carboxylation** is the addition of a carboxyl group (-COOH) to a molecule, a reaction crucial in processes like photosynthesis (carbon fixation) or the synthesis of certain proteins (e.g., clotting factors). - This chemical modification is not directly involved in the series of transformations that convert progesterone into **glucocorticoids**. *None of the options* - This option is incorrect because **hydroxylation** is indeed a fundamental chemical process in the conversion of progesterone to glucocorticoids.

Question 297: What is the immediate source of energy for cellular processes?

A. Cori's cycle
B. HMP
C. ATP (Correct Answer)
D. TCA cycle

Explanation: ***ATP*** - **Adenosine triphosphate (ATP)** is the direct and immediate source of energy for almost all cellular processes, including **muscle contraction**, **active transport**, and **biosynthesis**. - Its high-energy phosphate bonds release energy upon hydrolysis, driving various cellular functions. *Cori's cycle* - The **Cori cycle** involves the interconversion of **lactate** and **glucose** between the muscle and the liver to regenerate glucose stores. - It is an important metabolic pathway for glucose homeostasis during anaerobic conditions, but it does not directly provide immediate energy for cellular processes. *HMP* - The **Hexose Monophosphate Pathway (HMP)**, also known as the **pentose phosphate pathway**, primarily produces **NADPH** and **ribose-5-phosphate**. - While it generates NADPH for reductive biosynthesis and protects against oxidative stress, it is not an immediate source of energy. *TCA cycle* - The **Tricarboxylic Acid (TCA) cycle**, or Krebs cycle, is a central metabolic pathway that oxidizes **acetyl-CoA** to produce **ATP**, **NADH**, and **FADH2**. - While it is a major producer of ATP, it is not the *immediate* source; instead, it generates the precursors that fuel oxidative phosphorylation to produce ATP.

Question 298: Which organelle produces and destroys H2O2?

A. Peroxisome (Correct Answer)
B. Lysosome
C. Golgi body
D. Ribosome

Explanation: ***Peroxisome*** - **Peroxisomes** are organelles that both produce and break down **hydrogen peroxide (H2O2)** during metabolic processes. - They contain **oxidases** (such as D-amino acid oxidase and urate oxidase) that produce H2O2 as a byproduct during oxidation reactions. - They also contain the enzyme **catalase** that converts H2O2 into water and oxygen, protecting the cell from oxidative damage. - This dual function makes peroxisomes unique in H2O2 metabolism. *Lysosome* - **Lysosomes** are responsible for breaking down waste materials and cellular debris through **hydrolytic enzymes**. - They are primarily involved in **cellular digestion** and waste removal, not H2O2 metabolism. *Golgi body* - The **Golgi apparatus** modifies, sorts, and packages proteins and lipids for secretion or delivery to other organelles. - It is crucial for **protein trafficking** and glycosylation, but does not produce or destroy H2O2. *Ribosome* - **Ribosomes** are responsible for **protein synthesis** (translation) based on genetic information carried by mRNA. - They are involved in the assembly of amino acids into proteins, not the metabolism of hydrogen peroxide.

Question 299: What is the theoretical maximum number of ATPs generated from the Krebs cycle per glucose molecule?

A. 24 ATPs
B. 20 ATPs (Correct Answer)
C. 12 ATPs
D. 30 ATPs

Explanation: ***20 ATPs*** - Each **glucose molecule** yields two molecules of **acetyl-CoA** which enter the Krebs cycle. - Each turn of the **Krebs cycle** generates **3 NADH, 1 FADH2, and 1 GTP** (equivalent to 1 ATP). - Using modern **P/O ratios**: 3 NADH × 2.5 = 7.5 ATP, 1 FADH2 × 1.5 = 1.5 ATP, 1 GTP = 1 ATP, totaling **10 ATP per acetyl-CoA**. - Since two acetyl-CoA molecules are produced per glucose, the total is **2 × 10 = 20 ATPs** from the Krebs cycle alone. *24 ATPs* - This value is based on **older P/O ratios** (3 ATP per NADH, 2 ATP per FADH2), which have been revised in modern biochemistry. - While historically taught, current understanding of the **electron transport chain** efficiency yields lower ATP values per NADH and FADH2. *12 ATPs* - This represents the ATP yield from **one turn** of the **Krebs cycle** (or one acetyl-CoA molecule) using older P/O ratios, not a complete glucose molecule. - A single glucose molecule produces **two acetyl-CoA** molecules, each initiating a separate turn of the cycle. *30 ATPs* - This value typically reflects the theoretical maximum **total ATP** generated from **complete oxidation** of **one glucose molecule**, including contributions from **glycolysis** and the **electron transport chain**. - The Krebs cycle alone contributes only a portion of this total; 30 ATPs includes ATP from all stages of glucose metabolism.

Question 300: What is the mechanism of action of Atractyloside?

A. Inhibitor of oxidative phosphorylation (Correct Answer)
B. Uncoupler of oxidative phosphorylation
C. Inhibitor of complex III of the electron transport chain
D. Inhibitor of complex I of the electron transport chain

Explanation: ***Inhibitor of oxidative phosphorylation*** - **Atractyloside** is a potent **inhibitor of oxidative phosphorylation** by binding to and blocking the adenine nucleotide translocase (ANT) protein. - By inhibiting **ANT**, Atractyloside prevents the exchange of **ADP into the mitochondrial matrix** and ATP out, thereby halting ATP synthesis. *Uncoupler of oxidative phosphorylation* - **Uncouplers** dissipate the **proton gradient** across the inner mitochondrial membrane, allowing electron transport to continue without ATP synthesis. - Examples of uncouplers include **dinitrophenol (DNP)** and **thermogenin**, which act by increasing membrane permeability to protons. *Inhibitor of complex III of the electron transport chain* - Inhibitors of **Complex III** (cytochrome bc1 complex) block the transfer of electrons from **ubiquinone (CoQ)** to cytochrome c. - Examples include **antimycin A** and myxothiazol, which lead to an accumulation of reduced ubiquinone and a halt in electron flow. *Inhibitor of complex I of the electron transport chain* - **Complex I inhibitors** block the transfer of electrons from **NADH to ubiquinone (CoQ)** in the electron transport chain. - **Rotenone** and **amytal** are well-known inhibitors that prevent the pumping of protons and reduce ATP synthesis downstream.

Practice by Chapter

Bioenergetics and Thermodynamics

Practice Questions

ATP as Energy Currency

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Tricarboxylic Acid Cycle

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Electron Transport Chain

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Oxidative Phosphorylation

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Mitochondrial Diseases

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Uncouplers and Inhibitors of Oxidative Phosphorylation

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Shuttle Systems: Malate-Aspartate and Glycerol-Phosphate

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Energy Yield from Nutrients

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Metabolic Rate and Basal Metabolism

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Brown Adipose Tissue and Thermogenesis

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Oxygen Toxicity and Free Radicals

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