Prescott L F
Int J Clin Pharmacol Res. 1983;3(6):437-41.
Many compounds, including established drugs, cause liver damage through biotransformation to reactive cytotoxic metabolites which bind covalently to hepatic macromolecules. The forms of expression of such injury include acute necrosis, chronic hepatitis, cirrhosis and neoplasia. Hepatotoxicity depends on the balance between metabolic activation and inactivation and reduced glutathione protects against the toxicity of some agents by trapping their reactive electrophilic metabolites. Toxicity is usually increased by induction and decreased by inhibition of hepatic microsomal enzymes.
许多化合物，包括已有的药物，通过生物转化形成具有细胞毒性的活性代谢产物，这些代谢产物与肝脏大分子共价结合，从而导致肝损伤。这种损伤的表现形式包括急性坏死、慢性肝炎、肝硬化和肿瘤形成。肝毒性取决于代谢活化与失活之间的平衡，还原型谷胱甘肽通过捕获活性亲电代谢产物来保护机体免受某些药物的毒性作用。通常，肝微粒体酶的诱导会增加毒性，而抑制则会降低毒性。
