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© 1984 Oxford University Press

research-article

Paradoxical Effects of Perturbation of Intracellular Levels of Glutathione on Halothane-Induced Hepatotoxicity in Hyperthyroid Rats1

ADALINE C. SMITH2, ROBERT C. JAMES3, M. LAWRENCE BERMAN and RAYMOND D. HARBISON3,4

Departments of Pharmacology and Anesthesiology, Vanderbilt Medical Center Nashville, Tennessee 37203

Paradoxical Effects of Perturbation of Intracellular Levels of Glutathione on Halothane-Induced Hepatotoxicity in Hyperthyroid Rats. SMITH, A. C., JAMES, R. C., BERMAN, M. L., AND HARBISON, R. D. (1984). Fundam. Appl. Toxicol. 4, 221–230. Exposure of hyperthyroid rats to halothane results in a centrilobular necrosis of the liver and an 11-fold increase in serum glutamate–pyruvate transaminase (SGPT) levels. These effects are not seen in euthyroid animals. Paradoxically, administration of diethylmaleate to hyperthyroid rats significantly decreased the levels of hepatic glutathione and blocked the halothane-induced hepatic necrosis as well as decreased the elevation of SGPT. In contrast, pretreatment of animals with N-acetylcysteine, an intracellular sulfhydryl repletor, significantly increased the severity of the halothane-induced hepatic necrosis and increased the elevation of SGPT. Similarly, cysteamine, another intracellular sulfhydryl repletor, also exacerbated halothane-induced liver injury. Halothane-induced hepatotoxicity is at least in part apparently regulated by cellular glutathione levels. Paradoxically, glutathione seems to be involved in the bioactivation rather than the detoxification of halothane.


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