Energy Production and Metabolism — MCQs
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Mechanism of inhibition caused by cyanide and carbon monoxide poisoning involves inhibition of which enzyme?
The image shows the world's fastest athlete. Which of the following is used by his muscles for meeting energy demands to create world records in seconds?
Increased H+ ions in the intermembrane space of mitochondria are due to?
Type IV complex of ETC is inhibited by
All are cofactors for Dehydrogenase except:
What is the mechanism of cyanide poisoning?
Which protein secreted by adipocytes prevents obesity?
Low insulin to glucagon ratio leads to increase in the activity of
Glutathione is maintained in reduced state by the help of ?
All are sources of free radicals except -
Energy Production and Metabolism Indian Medical PG Practice Questions and MCQs
Question 221: Mechanism of inhibition caused by cyanide and carbon monoxide poisoning involves inhibition of which enzyme?
- A. Succinate dehydrogenase
- B. Cytochrome C oxidase (Correct Answer)
- C. NADH dehydrogenase
- D. Cytochrome C oxidoreductase
Explanation: ***Cytochrome C oxidase*** - Cyanide and carbon monoxide are **powerful inhibitors of Cytochrome C oxidase (Complex IV)** in the electron transport chain. - Cyanide binds to the **ferric iron (Fe³⁺)** in Complex IV, while carbon monoxide also binds to Complex IV, preventing oxygen from binding. - Inhibition of Complex IV **stops the transfer of electrons to oxygen**, halting the entire process of oxidative phosphorylation and cellular respiration, leading to **cellular hypoxia and energy deficit**. *Incorrect: NADH dehydrogenase* - This enzyme, also known as Complex I, is primarily inhibited by compounds like **Rotenone** and **Amytal**. - While crucial for the ETC, it is not the target of carbon monoxide or cyanide. *Incorrect: Succinate dehydrogenase* - This enzyme, known as Complex II, is an integral part of both the ETC and the Krebs cycle. - It is specifically inhibited by compounds like **Malonate** and is not the primary target in cyanide or carbon monoxide poisoning. *Incorrect: Cytochrome C oxidoreductase* - This enzyme represents Complex III (also called the Cytochrome bc1 complex). - It transfers electrons from ubiquinone to cytochrome C, but its inhibition is not the primary mechanism of action for cyanide or carbon monoxide, which directly target Complex IV.
Question 222: The image shows the world's fastest athlete. Which of the following is used by his muscles for meeting energy demands to create world records in seconds?
- A. Phosphofructokinase
- B. Glucose 1-phosphate
- C. Creatine phosphokinase
- D. Phosphocreatine (Correct Answer)
Explanation: ***Phosphocreatine*** - **Phosphocreatine** is a high-energy phosphate compound stored in muscle cells, providing the most rapid source of ATP regeneration for short, intense bursts of activity lasting seconds. - During explosive activities like sprinting (0-10 seconds), the enzyme **creatine kinase** rapidly transfers a phosphate group from phosphocreatine to ADP, re-synthesizing ATP almost instantaneously. - This **phosphagen system** (ATP-PC system) is the primary energy source for world-record sprints, allowing for maximal power output before glycolysis can ramp up. *Phosphofructokinase* - **Phosphofructokinase (PFK)** is a key regulatory enzyme in glycolysis, not an energy substrate itself. - While glycolysis provides ATP for sustained high-intensity exercise (10 seconds to 2 minutes), it is significantly slower than the phosphocreatine system. - PFK catalyzes the rate-limiting step of glycolysis but does not directly provide the immediate energy for explosive movements in seconds. *Glucose 1-phosphate* - **Glucose 1-phosphate** is an intermediate in glycogenolysis (glycogen breakdown) and glycogen synthesis. - It must be converted to glucose 6-phosphate and then proceed through glycolysis to generate ATP, which takes longer than direct phosphocreatine utilization. - This pathway supports energy production but is not the immediate source for explosive power in seconds. *Creatine phosphokinase* - **Creatine phosphokinase (CPK)** or **creatine kinase (CK)** is the enzyme that catalyzes the transfer of phosphate from phosphocreatine to ADP. - While essential for the process, it is the enzyme facilitator, not the energy substrate itself. - The question asks what is "used" for energy, which refers to the substrate (phosphocreatine), not the enzyme.
Question 223: Increased H+ ions in the intermembrane space of mitochondria are due to?
- A. Decreased ATP synthase activity
- B. Reduced proton pumping
- C. Impaired inner mitochondrial membrane integrity
- D. Increased electron transport chain activity (Correct Answer)
Explanation: ***Increased electron transport chain activity*** - The **electron transport chain (ETC)** complexes (I, III, and IV) actively pump **protons (H+)** from the mitochondrial matrix into the intermembrane space during electron transfer. - **Increased ETC activity** directly causes more protons to be pumped, creating a higher H+ concentration in the intermembrane space. - This is the **primary mechanism** for establishing the proton-motive force used in ATP synthesis. *Decreased ATP synthase activity* - While decreased ATP synthase activity would cause **passive accumulation** of protons in the intermembrane space (since fewer H+ flow back through ATP synthase), it does **not actively increase** proton pumping. - The question asks what causes the **increase** in H+ ions, which requires active transport by the ETC, not passive accumulation. - This option confuses the consequence (accumulation) with the cause (active pumping). *Reduced proton pumping* - **Reduced proton pumping** by the ETC would lead to a **decrease** in H+ concentration in the intermembrane space, as fewer protons are being actively transported. - This produces the opposite effect of what the question describes. *Impaired inner mitochondrial membrane integrity* - **Impaired membrane integrity** would cause protons to **leak back** into the mitochondrial matrix, dissipating the proton gradient. - This would **decrease**, not increase, the H+ concentration in the intermembrane space. - This is seen in uncoupling conditions where the membrane becomes permeable to protons.
Question 224: Type IV complex of ETC is inhibited by
- A. Antimycin
- B. Oligomycin
- C. CO2
- D. Cyanide (Correct Answer)
Explanation: ***Cyanide*** - **Cyanide** is a potent inhibitor of **cytochrome c oxidase (Complex IV)** in the electron transport chain, binding to its ferric iron center and preventing the reduction of oxygen to water. - This inhibition effectively blocks electron flow, leading to a rapid cessation of ATP production and cellular respiration. *Antimycin* - **Antimycin A** specifically inhibits **Complex III (cytochrome bc1 complex)** of the electron transport chain. - It binds to the Qn site of Complex III, preventing the transfer of electrons from reduced ubiquinone to cytochrome c. *Oligomycin* - **Oligomycin** is an inhibitor of **ATP synthase (Complex V)**, not Complex IV. - It blocks the flow of protons through the Fo subunit of ATP synthase, thereby inhibiting ATP synthesis, but it does not directly affect electron transport itself. *CO2* - **CO2** is a waste product of cellular respiration and is not an inhibitor of any complex within the electron transport chain. - While high levels of CO2 can affect pH and cellular function, it does not directly interfere with the catalytic activity of ETC complexes.
Question 225: All are cofactors for Dehydrogenase except:
- A. SAM (Correct Answer)
- B. NADP
- C. NAD
- D. FAD
Explanation: ***SAM*** - **S-adenosylmethionine (SAM)** is a cofactor involved in **methyl group transfer reactions**, carried out by enzymes known as methyltransferases. - Dehydrogenase enzymes catalyze **redox reactions**, typically involving the transfer of hydride ions, and thus do not utilize SAM as a cofactor. *NADP* - **Nicotinamide adenine dinucleotide phosphate (NADP)** is a crucial coenzyme for many **dehydrogenase reactions**, particularly in **anabolic pathways** like fatty acid synthesis and the pentose phosphate pathway. - It acts as an **electron carrier**, accepting or donating hydride ions. *NAD* - **Nicotinamide adenine dinucleotide (NAD)** is a highly common coenzyme for numerous **dehydrogenase enzymes**, especially in **catabolic pathways** such as glycolysis, the Krebs cycle, and oxidative phosphorylation. - It functions as an **electron acceptor** or donor in redox reactions. *FAD* - **Flavin adenine dinucleotide (FAD)** is a coenzyme derived from **riboflavin (Vitamin B2)** and is associated with various dehydrogenase enzymes, particularly those involved in **electron transport** and fatty acid oxidation. - FAD can accept two hydrogen atoms (one hydride and one proton) to become FADH₂.
Question 226: What is the mechanism of cyanide poisoning?
- A. Inhibition of cytochrome oxidase (Correct Answer)
- B. Inhibition of complex I
- C. Inhibition of cytochrome C
- D. Inhibition of carbonic anhydrase
Explanation: ***Inhibition of cytochrome oxidase*** - Cyanide rapidly binds to the **ferric iron (Fe3+)** in the **heme a3 component of cytochrome c oxidase** (Complex IV) in the mitochondrial electron transport chain. - This binding completely inhibits the enzyme's ability to transfer electrons to oxygen, thereby **halting cellular respiration** and ATP production. *Inhibition of complex I* - **Rotenone** and **barbiturates** are known inhibitors of **Complex I** (NADH dehydrogenase), not cyanide. - While inhibition of Complex I also disrupts the electron transport chain, it is not the primary mechanism of cyanide toxicity. *Inhibition of cytochrome C* - **Cytochrome C** is an electron carrier between Complex III and Complex IV, but it is not the direct target of cyanide. - Cytochrome C itself is not inhibited; rather, its function is compromised because **cytochrome c oxidase (Complex IV)**, which accepts electrons from it, is inhibited by cyanide. *Inhibition of carbonic anhydrase* - **Carbonic anhydrase**, an enzyme involved in CO2 transport and pH regulation, is inhibited by drugs like **acetazolamide**. - Its inhibition does not directly affect the mitochondrial electron transport chain or cause the rapid cellular hypoxia seen in cyanide poisoning.
Question 227: Which protein secreted by adipocytes prevents obesity?
- A. Galanin
- B. Neuropeptide Y
- C. Cathepsin
- D. Leptin (Correct Answer)
Explanation: ***Leptin*** - **Leptin** is a hormone secreted by **adipocytes** (fat cells) that plays a crucial role in long-term energy balance and appetite suppression. - It signals the brain about the body's energy stores, leading to decreased food intake and increased energy expenditure, and thus **preventing obesity**. *Galanin* - **Galanin** is a neuropeptide that has been shown to **stimulate food intake**, particularly fat consumption. - It is associated with **increased appetite** and **obesity**, rather than its prevention. *Neuropeptide Y* - **Neuropeptide Y (NPY)** is a potent **orexigenic** (appetite-stimulating) peptide primarily found in the hypothalamus. - Its activation leads to **increased food intake** and **decreased energy expenditure**, promoting weight gain and obesity. *Cathepsin* - **Cathepsins** are a family of **proteolytic enzymes** found in lysosomes. - They are involved in protein degradation and other cellular processes, but they are not directly involved in the prevention of obesity through appetite regulation or energy balance.
Question 228: Low insulin to glucagon ratio leads to increase in the activity of
- A. Hexokinase
- B. Glucokinase
- C. Glucose-6-phosphatase (Correct Answer)
- D. Pyruvate kinase
Explanation: ***Glucose-6-phosphatase*** - A low **insulin to glucagon ratio** signals a state of **low blood glucose**, leading to increased **glucagon** secretion. - Glucagon activates **gluconeogenesis** and **glycogenolysis** in the liver, and **glucose-6-phosphatase** is a key enzyme in the final step of both pathways, releasing free glucose into the bloodstream. *Hexokinase* - This enzyme is responsible for the **phosphorylation of glucose in most tissues** to trap it within the cell for glycolysis. - Its activity is generally high during periods of **high glucose and insulin levels** to promote glucose utilization. *Glucokinase* - This is an isoform of hexokinase found in the **liver and pancreatic beta cells**, with a higher Km for glucose, meaning it is active primarily at **high glucose concentrations**. - Its activity is increased by **insulin**, promoting glucose uptake and utilization in times of plenty. *Pyruvate kinase* - This enzyme catalyzes the final step of **glycolysis**, converting phosphoenolpyruvate to pyruvate. - Its activity is stimulated by **insulin** and inhibited by **glucagon**, reflecting its role in glucose breakdown, not production.
Question 229: Glutathione is maintained in reduced state by the help of ?
- A. Transamination
- B. HMP shunt (Correct Answer)
- C. Uronic acid pathway
- D. Glycogenesis
Explanation: ***HMP shunt*** - The **hexose monophosphate (HMP) shunt** produces **NADPH**, which is crucial for reducing **oxidized glutathione** back to its reduced form via **glutathione reductase**. - **Reduced glutathione** protects cells from **oxidative damage** by detoxifying harmful **reactive oxygen species.** *Transamination* - **Transamination** is a process involving the transfer of an **amino group** from an amino acid to a keto acid. - This pathway is primarily involved in **amino acid metabolism** and the synthesis of **non-essential amino acids**, not directly in glutathione reduction. *Uronic acid pathway* - The **uronic acid pathway** is involved in the synthesis of **glycolipids**, **sugars**, and **vitamin C** (in some animals). - It does not directly produce **NADPH** or enzymes necessary for maintaining **glutathione** in its reduced state. *Glycogenesis* - **Glycogenesis** is the process of synthesizing **glycogen** from **glucose** for storage, typically occurring in the liver and muscles. - This pathway is involved in **glucose storage** and **energy regulation**, not in the **redox state of glutathione**.
Question 230: All are sources of free radicals except -
- A. Glutathione (Correct Answer)
- B. Nitric oxide
- C. Myeloperoxidase
- D. Fenton's reaction
Explanation: ***Glutathione*** - **Glutathione** is a powerful **antioxidant** that helps to neutralize free radicals, not produce them. - It plays a crucial role in protecting cells from **oxidative damage**. *Nitric oxide* - **Nitric oxide (NO)** is a free radical itself, containing an unpaired electron. - It can lead to the formation of other reactive nitrogen species, contributing to **oxidative stress**. *Myeloperoxidase* - **Myeloperoxidase (MPO)** is an enzyme primarily found in neutrophils that produces powerful free radicals like **hypochlorous acid (HOCl)**, a highly reactive oxidant. - This process is essential for the immune system's ability to kill invading pathogens. *Fenton's reaction* - **Fenton's reaction** is a key chemical process that generates highly reactive **hydroxyl radicals (•OH)** from hydrogen peroxide in the presence of ferrous iron (Fe2+). - This reaction is a significant source of oxidative damage in biological systems.
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