Cell injury: free radical injury: practice question

A Pathology 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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Pathology · Cell injury: free radical injury

Sample item

A worker in a chemical plant is exposed to carbon tetrachloride vapour and later develops centrilobular hepatic necrosis with fatty change. What is the principal mechanism of hepatocyte injury?

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

The answer and the reasoning

C. Conversion by cytochrome P-450 into the trichloromethyl free radical, causing membrane lipid peroxidation

Carbon tetrachloride is metabolised in the smooth endoplasmic reticulum by P-450 to CCl3, a free radical. It attacks polyunsaturated membrane lipids, producing lipid peroxidation, loss of lipoprotein export and centrilobular necrosis with steatosis. The centrilobular zone is affected because P-450 activity is highest there.

Option by option

  • A. Direct inhibition of mitochondrial cytochrome oxidase

    Cytochrome oxidase inhibition is the mechanism of cyanide poisoning.

  • B. Binding to tubulin with arrest of hepatocyte mitosis

    Tubulin binding and mitotic arrest is the action of colchicine and vinca alkaloids.

  • C. Conversion by cytochrome P-450 into the trichloromethyl free radical, causing membrane lipid peroxidation (correct)

    Correct. The CCl3 radical causes autocatalytic lipid peroxidation of cell membranes.

  • D. Depletion of glutathione by an electrophilic metabolite

    Glutathione depletion by the metabolite NAPQI explains paracetamol hepatotoxicity.

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 Pathology question

What is the answer to this Pathology question?

The best answer is C, Conversion by cytochrome P-450 into the trichloromethyl free radical, causing membrane lipid peroxidation. Carbon tetrachloride is metabolised in the smooth endoplasmic reticulum by P-450 to CCl3, a free radical.

Why is "Direct inhibition of mitochondrial cytochrome oxidase" not the answer?

Cytochrome oxidase inhibition is the mechanism of cyanide poisoning.

Why is "Binding to tubulin with arrest of hepatocyte mitosis" not the answer?

Tubulin binding and mitotic arrest is the action of colchicine and vinca alkaloids.

Why is "Depletion of glutathione by an electrophilic metabolite" not the answer?

Glutathione depletion by the metabolite NAPQI explains paracetamol hepatotoxicity.

What concept does this question test?

It tests Cell injury: free radical injury in Pathology. It attacks polyunsaturated membrane lipids, producing lipid peroxidation, loss of lipoprotein export and centrilobular necrosis with steatosis. The centrilobular zone is affected because P-450 activity is highest there.

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 Cell injury: free radical injury?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology 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.