Pulmonary Toxicity of Carbon Tetrachloride
In the current view of the mechanism of CC14-induced hepatic necrosis, a free-radical metabolite presumably is generated in the liver during the complexing of CC14 with cytochrome P-450 and the subsequent reduction of the complex by NADPH and cytochrome P-450 reductase (e.g., see Reiner and Uehleke 1971; D’Acosta et al. 1973; Recknagel and Glende 1973; Sipes et al. 1977; Masuda and Murano 1978). The highly reactive free-radical is believed to be the actual toxic species causing hepatocellular damage, either by stimulating lipid peroxidation (e.g., see Recknagel and Ghoshal 1966; Slater 1972; Recknagel and Glende 1973) or by binding covalently to essential cellular macromolecules (e.g., see Reynolds 1967; Rao and Recknagel 1969; Castro and Gomez 1972; Recknagel and Glende 1973; Villarruel et al. 1977) or possibly by both mechanisms.
KeywordsCarbon Tetrachloride Pulmonary Toxicity Lung Slice CCl4 Treatment Lung Microsome
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