Glutathione and Detoxification — MCQs
Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
Which of the following is NOT true regarding the role of NAD+?
The following are major free radical scavengers except:
All of the following are true about glutathione, except:
A patient presents to the emergency department with a history of ingestion of ten tablets of paracetamol. He has developed oliguria and liver function tests show deranged values. In the context of paracetamol overdose, which of the following can be used in the management of this condition?
Which of the following is a tripeptide?
Ammonia is detoxified in brain by:
Ammonia is detoxified in brain to :
Kreb's cycle and urea cycle are linked by-
In G6PD deficiency, which enzyme's function is MOST directly impaired due to decreased NADPH availability, leading to reduced protection against oxidative stress?
Glutathione and Detoxification Indian Medical PG Practice Questions and MCQs
Question 1: Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
- A. Co-Q
- B. Cytochrome 'C'
- C. NAPQI (Correct Answer)
- D. N-acetylcysteine
Explanation: ***NAPQI*** - **N-acetyl-p-benzoquinone imine (NAPQI)** is a highly reactive and toxic metabolite produced during acetaminophen metabolism, especially in overdose situations [1, 3]. - When glutathione stores are depleted due to excessive NAPQI formation, this metabolite covalently binds to hepatic macromolecules, causing **hepatocellular damage and necrosis** [1, 3].*N-acetylcysteine* - **N-acetylcysteine (NAC)** is the antidote for acetaminophen overdose, not the toxic metabolite itself [2, 3]. - NAC works by replenishing hepatic **glutathione stores**, which helps detoxify NAPQI and prevent liver injury [2, 3].*Co-Q* - **Coenzyme Q10 (CoQ10)** is an endogenous antioxidant and electron carrier in the mitochondrial respiratory chain. - It is not a metabolite of acetaminophen and plays no direct role in acetaminophen-induced liver toxicity.*Cytochrome 'C'* - **Cytochrome c** is a protein involved in the electron transport chain in mitochondria and plays a critical role in apoptosis. - While cellular damage from NAPQI can eventually lead to cytochrome c release and apoptosis, cytochrome c itself is not a metabolite of acetaminophen or the direct cause of toxicity.
Question 2: Which of the following is NOT true regarding the role of NAD+?
- A. Acts as an electron carrier
- B. Functions as an antioxidant (Correct Answer)
- C. Participates in glycolysis
- D. Involved in TCA cycle
Explanation: ***Functions as an antioxidant*** - **NAD+** primarily functions as an **electron carrier** in redox reactions, not as an antioxidant that directly neutralizes reactive oxygen species. - While it plays a role in maintaining cellular redox balance, its direct function is not scavenging free radicals like **glutathione** or **vitamins C and E**. *Acts as an electron carrier* - **NAD+** is a crucial coenzyme that accepts electrons and protons during metabolic reactions, converting into **NADH**. - **NADH** then donates these electrons to the **electron transport chain** to generate **ATP**. *Participates in glycolysis* - In glycolysis, **NAD+** is reduced to **NADH** during the oxidation of **glyceraldehyde-3-phosphate** to **1,3-bisphosphoglycerate**. - This step is vital for producing **ATP** and regenerating **NAD+** for continued glycolytic flux. *Involved in TCA cycle* - **NAD+** is reduced to **NADH** at several steps in the **TCA cycle**, including the conversion of **isocitrate to α-ketoglutarate**, **α-ketoglutarate to succinyl CoA**, and **malate to oxaloacetate**. - These **NADH** molecules are then funneled into the **electron transport chain** for oxidative phosphorylation.
Question 3: The following are major free radical scavengers except:
- A. Glutathione
- B. Catalase
- C. Glutamine (Correct Answer)
- D. Superoxide dismutase
Explanation: ***Glutamine*** - **Glutamine** is an amino acid primarily involved in **protein synthesis**, immune function, and as a precursor for neurotransmitters, but it is not a direct antioxidant or free radical scavenger. - While it plays a role in maintaining cellular health, it does not directly neutralize **reactive oxygen species** like other listed compounds. *Glutathione* - **Glutathione** is a major endogenous antioxidant, directly neutralizing **free radicals** and participating in detoxification processes. - It's a key component of the **glutathione redox cycle**, protecting cells from oxidative damage. *Catalase* - **Catalase** is an enzyme that catalyzes the decomposition of hydrogen peroxide to water and oxygen, thus protecting cells from **oxidative damage**. - It is particularly important in neutralizing **reactive oxygen species** generated during metabolic processes. *Superoxide dismutase* - **Superoxide dismutase (SOD)** is an enzyme that catalyzes the dismutation of the **superoxide radical** into oxygen and hydrogen peroxide. - It is a crucial primary antioxidant defense against **oxidative stress**.
Question 4: All of the following are true about glutathione, except:
- A. It is co-factor of various enzymes
- B. It converts hemoglobin to methemoglobin (Correct Answer)
- C. It is a tripeptide
- D. It conjugates xenobiotics
Explanation: ***It converts hemoglobin to methemoglobin*** - Glutathione is a **reducing agent** that helps protect hemoglobin from oxidation, thus **preventing** the formation of methemoglobin. - **Methemoglobin** occurs when the iron in hemoglobin is oxidized from the ferrous (Fe2+) to the ferric (Fe3+) state, which is a process glutathione actively counters. *It is co-factor of various enzymes* - Glutathione serves as a crucial **co-factor** for several enzymes, including **glutathione peroxidase**, which plays a vital role in antioxidant defense. - It participates in various **detoxification reactions** and catalyzes the reduction of harmful reactive oxygen species. *It is a tripeptide* - Glutathione is indeed a **tripeptide** composed of three amino acids: **glutamate**, **cysteine**, and **glycine**. - Its unique structure enables its diverse biological functions, including its prominent role as an antioxidant. *It conjugates xenobiotics* - Glutathione plays a critical role in **detoxifying xenobiotics** (foreign compounds) by conjugating with them, making them more water-soluble and easier to excrete. - This process is mediated by **glutathione S-transferases**, which attach glutathione to various toxic compounds.
Question 5: A patient presents to the emergency department with a history of ingestion of ten tablets of paracetamol. He has developed oliguria and liver function tests show deranged values. In the context of paracetamol overdose, which of the following can be used in the management of this condition?
- A. N-acetylcysteine (Correct Answer)
- B. Dopamine
- C. Ursodeoxycholic acid
- D. Furosemide
Explanation: **Correct: N-acetylcysteine** - **N-acetylcysteine (NAC)** is the specific antidote for **paracetamol overdose**, working by replenishing **glutathione** stores in the liver. - Replenishing **glutathione** helps detoxify the toxic metabolite **N-acetyl-p-benzoquinone imine (NAPQI)**, preventing further **hepatic damage** and facilitating recovery in cases of **liver failure** and potential **renal damage** (oliguria). - Most effective when given within **8 hours** of ingestion, but remains beneficial even with **established hepatotoxicity** (as in this case with deranged LFTs). *Incorrect: Dopamine* - **Dopamine** is a **vasopressor** primarily used to increase **blood pressure** and **cardiac output** in conditions like **shock**. - While it might be used to support circulation in severe overdose complications, it does not directly treat the **paracetamol toxicity** itself. *Incorrect: Ursodeoxycholic acid* - **Ursodeoxycholic acid (UDCA)** is a **cholagogue** used in the management of **cholestatic liver diseases** (e.g., primary biliary cholangitis) by improving bile flow. - It has no role in the direct management of **acute liver failure** due to **paracetamol overdose**. *Incorrect: Furosemide* - **Furosemide** is a **loop diuretic** used to increase **urine output** in conditions like **fluid overload** or **heart failure**. - While **oliguria** is present, it is often a sign of **acute kidney injury** requiring supportive care, and furosemide would not address the underlying **toxic mechanism** of paracetamol.
Question 6: Which of the following is a tripeptide?
- A. Glutathione (Correct Answer)
- B. Angiotensin
- C. Glucagon
- D. Oxytocin
Explanation: ***Glutathione*** - **Glutathione** is a tripeptide composed of three amino acids: **glutamate**, **cysteine**, and **glycine**. - It plays a crucial role as an **antioxidant** in the body, protecting cells from damage by **free radicals**. *Angiotensin* - **Angiotensin** is a peptide hormone that causes **vasoconstriction** and an increase in **blood pressure**. - It is an **oligopeptide** (typically 8-10 amino acids) rather than a tripeptide. *Glucagon* - **Glucagon** is a peptide hormone produced by the **alpha cells** of the pancreas that raises **blood glucose levels**. - It is a **29-amino acid** polypeptide, much larger than a tripeptide. *Oxytocin* - **Oxytocin** is a hormone involved in social bonding and sexual reproduction, best known for its role in **childbirth** and **lactation**. - It is a **nonapeptide**, meaning it consists of nine amino acids.
Question 7: Ammonia is detoxified in brain by:
- A. Glutamine (Correct Answer)
- B. Creatinine
- C. Urea
- D. Uric acid
Explanation: ***Glutamine*** - Brain cells, particularly **astrocytes**, detoxify ammonia by converting it into glutamine using **glutamine synthetase**. - This process binds ammonia to **glutamate**, forming **glutamine**, which is less toxic and can be transported to the liver for further processing or used as a nitrogen source. *Creatinine* - Creatinine is a **metabolic waste product** primarily from muscle metabolism, derived from creatine phosphate. - It is eliminated mainly by the **kidneys** and plays no direct role in ammonia detoxification in the brain. *Urea* - Urea is the primary form of nitrogenous waste in humans and is produced in the **liver** via the **urea cycle**. - While it's the main way the body excretes ammonia, the brain itself does not perform the full urea cycle for detoxification. *Uric acid* - Uric acid is the end product of **purine metabolism** and is excreted primarily by the kidneys. - It is not involved in the direct detoxification of ammonia in the brain.
Question 8: Ammonia is detoxified in brain to :
- A. Urea
- B. GABA
- C. Glutamine (Correct Answer)
- D. Uric acid
Explanation: ***Glutamine*** - In the brain, **ammonia** is primarily detoxified through its conversion into **glutamine** by the enzyme **glutamine synthetase**. - This process is crucial for preventing **neurotoxicity** as ammonia can disrupt neuronal function and energy metabolism. *Urea* - **Urea** is the primary end product of **ammonia detoxification** in the **liver** through the **urea cycle**. - While urea can cross the blood-brain barrier, it is not the main mechanism for local ammonia detoxification within brain cells. *GABA* - **GABA (gamma-aminobutyric acid)** is an **inhibitory neurotransmitter** formed from **glutamate**. - It plays a vital role in neuronal signaling but is not directly involved in the detoxification of ammonia in the brain. *Uric acid* - **Uric acid** is the end product of **purine metabolism** and acts as an antioxidant. - It is not directly involved in the detoxification pathway of ammonia in the brain or any other organ.
Question 9: Kreb's cycle and urea cycle are linked by-
- A. Malate
- B. Succinate
- C. α-ketoglutarate
- D. Fumarate (Correct Answer)
Explanation: ***Fumarate*** - **Fumarate** is a key intermediate produced in the **urea cycle** during the conversion of argininosuccinate to arginine, which then enters the **Krebs cycle** to be converted into malate and then oxaloacetate. - This molecule acts as a direct link, allowing metabolic crosstalk between the two cycles. *Malate* - While **malate** is an intermediate in the Krebs cycle and is derived from fumarate, it is not the direct molecule that links the two cycles. - Malate is formed in the cytoplasm from fumarate but must be transported into the mitochondria to continue in the Krebs cycle. *α-ketoglutarate* - **α-ketoglutarate** is an important intermediate in the Krebs cycle involved in amino acid metabolism, but it does not directly link the urea cycle to the Krebs cycle. - It plays a role in nitrogen metabolism by accepting amino groups, but not in the *direct* transference of carbon skeletons between the cycles in the same way fumarate does. *Succinate* - **Succinate** is an intermediate of the Krebs cycle that is formed from succinyl CoA, but it does not directly participate in the urea cycle as a connecting molecule. - Its primary role is in **oxidative phosphorylation** as it is converted to fumarate by succinate dehydrogenase within the electron transport chain.
Question 10: In G6PD deficiency, which enzyme's function is MOST directly impaired due to decreased NADPH availability, leading to reduced protection against oxidative stress?
- A. Catalase
- B. Pyruvate kinase
- C. Superoxide dismutase
- D. Glutathione reductase (Correct Answer)
Explanation: ***Glutathione reductase*** - **G6PD deficiency** impairs the production of **NADPH** through the pentose phosphate pathway - **Glutathione reductase** is NADPH-dependent and reduces oxidized glutathione (GSSG) back to reduced glutathione (GSH) - Without adequate NADPH, glutathione reductase cannot maintain sufficient **GSH levels**, which is the primary antioxidant protecting RBCs from oxidative damage - This explains why G6PD deficiency leads to **hemolysis** when exposed to oxidative stressors (antimalarials, sulfonamides, fava beans) *Catalase* - **Catalase** decomposes hydrogen peroxide to water and oxygen, protecting cells from oxidative damage - While important for antioxidant defense, catalase does **not require NADPH** for its function - Its activity is not directly impaired by decreased NADPH in G6PD deficiency *Pyruvate kinase* - **Pyruvate kinase** catalyzes the final step of **glycolysis**, producing ATP - Its function is **completely independent** of NADPH levels - Pyruvate kinase deficiency causes a separate hemolytic anemia unrelated to oxidative stress or G6PD deficiency *Superoxide dismutase* - **Superoxide dismutase (SOD)** converts superoxide radicals to hydrogen peroxide and oxygen - SOD functions **independently of NADPH** and uses metal cofactors (Cu/Zn or Mn) - While part of antioxidant defense, it is not directly affected by G6PD deficiency
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