Which vitamin deficiency results from long-term recreational abuse of nitrous oxide?

Question

BlackTom AI · Accepted Answer

The question asks: Which vitamin deficiency results from long-term recreational abuse of nitrous oxide? Let's evaluate each option in turn.
Option 1: Niacin. Niacin deficiency leads to pellagra, characterized by dermatitis, diarrhea, dementia, and death in severe cases. This is not associated with nitrous oxide exposure, so this option is incorrect.
Option 2: Riboflavin. Riboflavin deficiency causes ariboflavinosis, with symptoms like sore throat, angular cheilitis, glossitis, and seborrheic dermatitis. There is no established link between nitrous oxide abuse and riboflavin deficiency, so this choice is not correct.
Option 3: Cobalamin. Cobalamin is vitamin B12. Chronic nitrous oxide exposure inactivates the B12-dependent enzyme methionine synthase by oxidizing the cobalt center of B12, leading to a functional B12 deficiency. This mechanism is well-documented in medical literature on nitrous oxide abuse, making this option correct.
Option 4: Ascorbic acid. Ascorbic acid is vitamin C, deficiency causing scurvy with symptoms like gum bleeding and poor wound healing. There is no direct, established effect of nitrous oxide on vitamin C status, so this option is incorrect.
In summary, while the other vitamins describe distinct deficiency syndromes unrelated to nitrous oxide, the unique, mechanism-based link between nitrous oxide exposure and vitamin B12 (cobalamin) inactivation makes option 3 the accurate choice for this question.

Which vitamin deficiency results from long-term recreational abuse of nitrous oxide?

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