One-Carbon Transfer Reactions — MCQs
What is the appropriate treatment for megaloblastic anemia with neurological symptoms?
Which of the following is not a precursor in the synthesis of pyrimidines?
Which vitamin deficiency leads to megaloblastic anemia?
Which drug is metabolized by glutathionation?
The cofactor vitamin B12 is required for the following conversion:
All are cofactors for Dehydrogenase except:
What is the mechanism of action of Methotrexate?
Amino acid required for conversion of norepinephrine to epinephrine:-
In the metabolism of xenobiotics, which of the following reactions does not occur in phase one?
Which one among the following essential amino acids is usually the "limiting" amino acid in most of the pulses?
One-Carbon Transfer Reactions Indian Medical PG Practice Questions and MCQs
Question 1: What is the appropriate treatment for megaloblastic anemia with neurological symptoms?
- A. Iron supplementation
- B. Folic acid with Hydroxycobalamin (Correct Answer)
- C. Vitamin B1 supplementation
- D. Folic Acid only
Explanation: Folic acid with Hydroxycobalamin - Neurological symptoms in megaloblastic anemia strongly suggest vitamin B12 deficiency, as folic acid alone can mask this deficiency and worsen neurological sequelae [3]. - Hydroxycobalamin is the preferred treatment for vitamin B12 deficiency, while folic acid addresses the megaloblastic hematopoiesis. Iron supplementation - This is used to treat iron deficiency anemia, which presents with microcytic or normocytic red blood cells, not megaloblastic changes [1]. - Iron supplementation would not address the neurological symptoms or the underlying B12 or folate deficiency. Vitamin B1 supplementation - Vitamin B1 (thiamine) deficiency is associated with conditions like beriberi and Wernicke-Korsakoff syndrome, characterized by neurological symptoms, but not megaloblastic anemia [4]. - Supplementation would not correct the underlying hematological abnormality or the specific neurological symptoms of B12 deficiency [4]. Folic Acid only - While folic acid is essential for DNA synthesis and would improve the hematological parameters of megaloblastic anemia, it does not treat vitamin B12 deficiency [2]. - Giving folic acid alone in the presence of B12 deficiency can lead to a worsening of neurological symptoms as it can correct the anemia but allow the neurological damage to progress [3].
Question 2: Which of the following is not a precursor in the synthesis of pyrimidines?
- A. Glutamine
- B. Carbon dioxide (CO2)
- C. Aspartic acid
- D. Thymidine (Correct Answer)
Explanation: ***Thymidine*** - **Thymidine** is a *nucleoside* consisting of deoxyribose and thymine. It is a *product* and a component of DNA, not a precursor in the *de novo synthesis* of pyrimidine bases. - While it can be incorporated into DNA via the *salvage pathway*, it does not serve as an initial building block for the pyrimidine ring itself. *Glutamine* - **Glutamine** provides the **nitrogen atoms** crucial for the formation of the pyrimidine ring, specifically N3 in the pyrimidine base. - It is a key donor of *amino groups* in various anabolic pathways, including nucleotide synthesis. *Carbon dioxide (CO2)* - **Carbon dioxide (CO2)** contributes one of the carbon atoms (C2) to the pyrimidine ring. - It combines with **ammonia** (derived from glutamine) to form **carbamoyl phosphate**, an essential intermediate. *Aspartic acid* - **Aspartic acid** provides four atoms (N1, C4, C5, C6) of the pyrimidine ring. - Its carbon skeleton and amino group are directly incorporated into the pyrimidine structure during the *de novo synthesis* pathway.
Question 3: Which vitamin deficiency leads to megaloblastic anemia?
- A. Riboflavin
- B. Folate (Correct Answer)
- C. Vitamin C
- D. Niacin
Explanation: ***Folate*** - **Folate** is essential for DNA synthesis; a deficiency impairs erythrocyte maturation, leading to the production of **large, immature red blood cells** (megaloblasts) [3]. - This vitamin deficiency also presents with symptoms like **fatigue, glossitis**, and neurologic manifestations are absent unlike vitamin B12 deficiency [1]. *Riboflavin* - **Riboflavin (Vitamin B2)** deficiency can cause **normocytic anemia**, but generally not megaloblastic anemia. - Its deficiency is mainly associated with **angular stomatitis, cheilosis**, and ocular symptoms. *Vitamin C* - **Vitamin C** deficiency (scurvy) is associated with impaired collagen synthesis, leading to **gingival bleeding, petechiae**, and poor wound healing. - While it can cause some anemia, it is typically **microcytic** due to impaired iron absorption if it affects iron metabolism, not megaloblastic [2]. *Niacin* - **Niacin (Vitamin B3)** deficiency causes **pellagra**, characterized by the "3 D's": **dermatitis, diarrhea, and dementia**. - It does not directly lead to megaloblastic anemia, as it is not involved in a critical step of DNA synthesis in the same way folate is.
Question 4: Which drug is metabolized by glutathionation?
- A. Nicotinic acid
- B. Fosfomycin
- C. Benzodiazepines
- D. Dapsone (Correct Answer)
Explanation: ***Dapsone***- **Dapsone** undergoes hepatic metabolism via **N-hydroxylation** by CYP450 enzymes (particularly CYP2E1 and CYP3A4), forming reactive **hydroxylamine metabolites**.- These reactive metabolites are toxic and can cause **methemoglobinemia** and **hemolysis**.- **Glutathione conjugation (glutathionation)** serves as an important **detoxification pathway** for these reactive dapsone metabolites [1].- Individuals with **glutathione deficiency** (such as G6PD deficiency) are at increased risk of dapsone-induced hemolytic anemia [2].*Fosfomycin*- **Fosfomycin** is primarily eliminated by the kidneys as an **unchanged drug** (up to 90% excreted unchanged in urine).- It undergoes **minimal hepatic metabolism** and does NOT undergo significant glutathionation.- Its primary route of elimination is **renal excretion** via glomerular filtration.*Benzodiazepines*- **Benzodiazepines** are primarily metabolized in the liver via **CYP450 enzymes** (Phase I oxidation) followed by **glucuronidation** (Phase II conjugation).- They do NOT undergo glutathionation as a significant metabolic pathway.*Nicotinic acid*- **Nicotinic acid** (niacin) undergoes conjugation with **glycine** to form nicotinuric acid and **methylation** to form N-methylnicotinamide.- It does NOT undergo glutathione conjugation.
Question 5: The cofactor vitamin B12 is required for the following conversion:
- A. Dopamine to Norepinephrine
- B. Propionyl CoA to methyl malonyl CoA
- C. Methyl malonyl CoA to succinyl CoA (Correct Answer)
- D. Homocysteine to cysteine
Explanation: ***Methyl malonyl CoA to succinyl CoA*** - **Vitamin B12**, in its active form **adenosylcobalamin**, is a crucial cofactor for the enzyme **methylmalonyl-CoA mutase**, which catalyzes the isomerization of **methylmalonyl-CoA to succinyl-CoA**. - This conversion is vital for the metabolism of **odd-chain fatty acids** and certain **amino acids**, allowing their entry into the **Krebs cycle**. *Dopamine to Norepinephrine* - This conversion is catalyzed by **dopamine beta-hydroxylase**, which requires **vitamin C** (ascorbate) and **copper** as cofactors, not vitamin B12. - It is a key step in the synthesis of **catecholamines** within the nervous system. *Propionyl CoA to methyl malonyl CoA* - This conversion is catalyzed by **propionyl-CoA carboxylase** and requires **biotin** as a cofactor, not vitamin B12. - This reaction is the first step in the metabolic pathway that leads to succinyl-CoA from odd-chain fatty acids. *Homocysteine to cysteine* - This conversion occurs via the **transsulfuration pathway** and requires **vitamin B6** (pyridoxal phosphate) as a cofactor, not vitamin B12. - The enzymes involved are **cystathionine β-synthase** and **cystathionine γ-lyase**, both B6-dependent. - Vitamin B12 is involved in the **remethylation** of homocysteine to methionine (not in transsulfuration to cysteine).
Question 6: 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 7: What is the mechanism of action of Methotrexate?
- A. Inhibition of Dihydrofolate reductase (Correct Answer)
- B. Inhibits pyrimidine synthesis
- C. Inhibits cell replication by acting on G phase of cell cycle
- D. Inhibits Thymidylate synthase
- E. Inhibits RNA polymerase
Explanation: ***Inhibition of Dihydrofolate reductase*** - **Methotrexate** is a **folate analog** that competitively inhibits **dihydrofolate reductase (DHFR)**, an enzyme essential for converting **dihydrofolate** to **tetrahydrofolate**. - This inhibition blocks the synthesis of **purines** and **pyrimidines**, thereby preventing DNA and RNA synthesis and ultimately inhibiting cell proliferation. *Inhibits pyrimidine synthesis* - While methotrexate ultimately inhibits pyrimidine synthesis by depleting tetrahydrofolate, its direct mechanism is not the inhibition of the pyrimidine synthesis pathway enzymes themselves. - Its primary action is upstream, by inhibiting DHFR. *Inhibits cell replication by acting on G phase of cell cycle* - Methotrexate primarily inhibits cells in the **S-phase** of the cell cycle, as it interferes with DNA synthesis. - It does not specifically target the G phase; rather, it affects cells that are actively attempting to replicate their DNA. *Inhibits Thymidylate synthase* - **Thymidylate synthase** is inhibited by drugs like **5-fluorouracil**, which directly blocks the conversion of **deoxyuridine monophosphate (dUMP)** to **deoxythymidine monophosphate (dTMP)**. - Methotrexate's effect on thymidylate synthesis is indirect, mediated by the depletion of the cofactor **N5,N10-methylene-tetrahydrofolate** due to DHFR inhibition. *Inhibits RNA polymerase* - **RNA polymerase** inhibition is the mechanism of drugs like **rifampin** (bacterial RNA polymerase) and **α-amanitin** (eukaryotic RNA polymerase). - Methotrexate does not directly inhibit RNA polymerase; its effects on RNA synthesis are secondary to depletion of nucleotide precursors through DHFR inhibition.
Question 8: Amino acid required for conversion of norepinephrine to epinephrine:-
- A. Lysine
- B. Tryptophan
- C. Methionine (Correct Answer)
- D. Phenylalanine
Explanation: ***Methionine*** - **Norepinephrine** is converted to **epinephrine** by the enzyme **phenylethanolamine N-methyltransferase (PNMT)**. - This enzyme uses **S-adenosylmethionine (SAM)** as a **methyl donor**, which is derived from methionine. *Lysine* - **Lysine** is an essential amino acid primarily involved in **protein synthesis**, **calcium absorption**, and the production of **carnitine**. - It does not directly participate in the methylation reaction converting norepinephrine to epinephrine. *Tryptophan* - **Tryptophan** is a precursor for **serotonin** and **niacin** synthesis. - It is not involved in the catecholamine synthesis pathway from norepinephrine to epinephrine. *Phenylalanine* - **Phenylalanine** is the initial amino acid in the **catecholamine synthesis pathway**, being converted to **tyrosine**, then to DOPA, dopamine, and norepinephrine. - While it's crucial for the synthesis *up to* norepinephrine, it is not directly involved in the *conversion of norepinephrine to epinephrine*.
Question 9: In the metabolism of xenobiotics, which of the following reactions does not occur in phase one?
- A. Reduction
- B. Hydrolysis
- C. Oxidation
- D. Conjugation (Correct Answer)
Explanation: ***Correct Answer: Conjugation*** - **Conjugation** reactions are characteristic of **Phase II metabolism**, NOT Phase I - In Phase II, a polar molecule (glucuronide, sulfate, acetyl, or glutathione) is added to the xenobiotic to increase water solubility and facilitate excretion - This process typically renders the xenobiotic inactive and more readily eliminated by the kidneys or bile - Common conjugation reactions include glucuronidation, sulfation, acetylation, and glutathione conjugation *Incorrect: Oxidation* - **Oxidation** is a primary **Phase I reaction**, primarily involving the cytochrome P450 (CYP450) enzyme system - Phase I oxidation introduces or exposes polar functional groups (-OH, -COOH, -NH2) - This makes the xenobiotic more reactive and prepares it for Phase II conjugation - Examples include hydroxylation, N-dealkylation, and O-dealkylation *Incorrect: Reduction* - **Reduction** reactions are also common in **Phase I metabolism** - Particularly important for compounds containing nitro groups, carbonyl groups, or azo compounds - These reactions can occur in various tissues, including the liver - Catalyzed by reductases such as cytochrome P450 reductase and other enzyme systems *Incorrect: Hydrolysis* - **Hydrolysis** is another key **Phase I reaction** that breaks down xenobiotics by adding water - Especially important for esters, amides, and other compounds with hydrolyzable bonds - Enzymes like esterases, amidases, and peptidases catalyze these reactions - Results in more polar metabolites that can undergo Phase II conjugation
Question 10: Which one among the following essential amino acids is usually the "limiting" amino acid in most of the pulses?
- A. Valine
- B. Threonine
- C. Methionine (Correct Answer)
- D. Lysine
Explanation: ***Methionine*** - In **pulses** (legumes), the sulfur-containing amino acids, primarily **methionine** and **cysteine**, are often the first limiting amino acids. - This means that the amount of protein synthesis that can occur is restricted by the availability of methionine, even if other essential amino acids are abundant. *Valine* - **Valine** is an essential branched-chain amino acid, but it is typically not the limiting amino acid in pulses. - It is more likely to be limiting in certain grains or in specific diets lacking a variety of protein sources. *Threonine* - **Threonine** is an essential amino acid that can be limiting in some cereals, but it is not typically the primary limiting amino acid in pulses. - Its deficiency is less common in a balanced diet including legumes. *Lysine* - **Lysine** is often the limiting amino acid in most **cereal grains** (e.g., wheat, corn, rice). - Pulses, however, are generally good sources of lysine, making its deficiency less likely when consumed.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free