Purine nucleotide cycle: myoadenylate deaminase deficiency: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Purine nucleotide cycle: myoadenylate deaminase deficiency

Sample item

A 20-year-old has fatigue and myalgia after exercise. Lactate rises normally, there is no myoglobinuria, and the post-exercise ammonia rise is blunted. Biopsy shows no staining for myoadenylate deaminase. Which reaction is blocked?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

C. Deamination of AMP to IMP, releasing ammonia

In the purine nucleotide cycle in exercising muscle, AMP is deaminated to IMP (myoadenylate deaminase), IMP is converted back to AMP via adenylosuccinate, releasing fumarate that replenishes TCA cycle intermediates. Loss of the first step blunts ammonia production and fumarate supply, causing exertional myalgia but sparing glycolysis.

Option by option

  • A. Conversion of IMP to adenylosuccinate using aspartate and GTP

    Adenylosuccinate synthetase is the next step in the cycle, and its loss would not stop ammonia formation.

  • B. Deamination of adenosine to inosine

    Adenosine deamination is performed by adenosine deaminase, whose deficiency causes one form of severe combined immunodeficiency.

  • C. Deamination of AMP to IMP, releasing ammonia (correct)

    The cycle begins with AMP deaminase, and its loss explains the blunted ammonia rise.

  • D. Oxidation of hypoxanthine to xanthine

    Xanthine oxidase acts later in purine catabolism and is unrelated to muscle ammonia release.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is C, Deamination of AMP to IMP, releasing ammonia. In the purine nucleotide cycle in exercising muscle, AMP is deaminated to IMP (myoadenylate deaminase), IMP is converted back to AMP via adenylosuccinate, releasing fumarate that replenishes TCA cycle intermediates.

Why is "Conversion of IMP to adenylosuccinate using aspartate and GTP" not the answer?

Adenylosuccinate synthetase is the next step in the cycle, and its loss would not stop ammonia formation.

Why is "Deamination of adenosine to inosine" not the answer?

Adenosine deamination is performed by adenosine deaminase, whose deficiency causes one form of severe combined immunodeficiency.

Why is "Oxidation of hypoxanthine to xanthine" not the answer?

Xanthine oxidase acts later in purine catabolism and is unrelated to muscle ammonia release.

What concept does this question test?

It tests Purine nucleotide cycle: myoadenylate deaminase deficiency in Biochemistry. Loss of the first step blunts ammonia production and fumarate supply, causing exertional myalgia but sparing glycolysis.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Purine nucleotide cycle: myoadenylate deaminase deficiency?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.