A worker exposed to carbon tetrachloride develops centrilobular hepatic necrosis. The initiating biochemical event occurs in the smooth endoplasmic reticulum of hepatocytes and involves:

• A CYP2E1-mediated conversion of CCl4 to the trichloromethyl radical (CCl3•) ✓
• B Glucuronidation of CCl4 by UDP-glucuronosyltransferases
• C Glutathione conjugation releasing a quinone imine
• D Direct solubilisation of mitochondrial membranes by intact CCl4

Explanation

Carbon tetrachloride is bioactivated by hepatic CYP2E1 into the trichloromethyl free radical, which initiates lipid peroxidation of endoplasmic reticulum membranes and destroys cellular machinery, causing fatty change and centrilobular necrosis. The parent compound itself is inert, so option D fails. Unlike paracetamol, the injury is radical-mediated rather than covalent adduct-mediated, which distinguishes the two classic toxicology models.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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