Question:hard
Which of the following is true?
Which of the following is true?
Show Hint
Three statements name the wrong enzyme or wrong inhibition type; find the antidote concept that holds.
Updated On: Jun 24, 2026
- Acetylcholinesterase inhibition by malathion can be reversed by increasing the level of atropine
- Sulphonamide inhibits folate reductase irreversibly
- Fluoroacetate competitively inhibits aconitase
- Ethanol acts by inhibiting aldehyde dehydrogenase when used in methanol poisoning
Show Solution
The Correct Option is D
Solution and Explanation
This statement-validity question requires checking each toxicology claim against the real mechanism and keeping the one that is closest to true.
Starting with the organophosphate option: malathion poisons acetylcholinesterase, and the antidote pairing is atropine for the muscarinic symptoms plus an oxime such as pralidoxime to actually free the enzyme. Atropine alone never reverses the enzyme block, so that statement collapses. Next, sulphonamides are structural mimics of para-aminobenzoic acid and inhibit dihydropteroate synthase in bacterial folate synthesis; folate (dihydrofolate) reductase is a different enzyme targeted by trimethoprim and methotrexate, so that claim is also wrong. Fluoroacetate is the classic example of lethal synthesis: it is converted into fluorocitrate which shuts down aconitase, but the action is not a reversible competitive inhibition, so that wording fails too.
That leaves the methanol antidote statement. Methanol itself is fairly harmless until alcohol dehydrogenase oxidises it to formaldehyde and then formic acid, which cause the metabolic acidosis and blindness. Ethanol is the traditional antidote because it competes for alcohol dehydrogenase and diverts the enzyme away from methanol, buying time for clearance. The printed wording names aldehyde dehydrogenase, which is a small inaccuracy, yet this option still expresses the only correct antidotal concept among the four, making it the best answer.
\[\boxed{\text{Ethanol competes for the enzyme in methanol poisoning (best answer)}}\]
Starting with the organophosphate option: malathion poisons acetylcholinesterase, and the antidote pairing is atropine for the muscarinic symptoms plus an oxime such as pralidoxime to actually free the enzyme. Atropine alone never reverses the enzyme block, so that statement collapses. Next, sulphonamides are structural mimics of para-aminobenzoic acid and inhibit dihydropteroate synthase in bacterial folate synthesis; folate (dihydrofolate) reductase is a different enzyme targeted by trimethoprim and methotrexate, so that claim is also wrong. Fluoroacetate is the classic example of lethal synthesis: it is converted into fluorocitrate which shuts down aconitase, but the action is not a reversible competitive inhibition, so that wording fails too.
That leaves the methanol antidote statement. Methanol itself is fairly harmless until alcohol dehydrogenase oxidises it to formaldehyde and then formic acid, which cause the metabolic acidosis and blindness. Ethanol is the traditional antidote because it competes for alcohol dehydrogenase and diverts the enzyme away from methanol, buying time for clearance. The printed wording names aldehyde dehydrogenase, which is a small inaccuracy, yet this option still expresses the only correct antidotal concept among the four, making it the best answer.
\[\boxed{\text{Ethanol competes for the enzyme in methanol poisoning (best answer)}}\]
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