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Pulmonary Toxicity of Carbon Tetrachloride

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Book cover Industrial and Environmental Xenobiotics

Part of the book series: Proceedings in Life Sciences ((LIFE SCIENCES))

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Abstract

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.

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© 1981 Springer-Verlag Berlin Heidelberg

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Boyd, M.R. (1981). Pulmonary Toxicity of Carbon Tetrachloride. In: Gut, I., Cikrt, M., Plaa, G.L. (eds) Industrial and Environmental Xenobiotics. Proceedings in Life Sciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68195-0_14

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  • DOI: https://doi.org/10.1007/978-3-642-68195-0_14

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-68197-4

  • Online ISBN: 978-3-642-68195-0

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