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- W2037904562 abstract "During aerobic incubations of rat liver microsomes containing a NADPH generating system, 1.54% of added carbon tetrachloride (14CCl4), and 3.05% of added Bromotrichloromethane (CBrCl3) could be recovered as the 2-oxothiazolidene-4-carboxylic acid derivative of phosgene. Actual nanomolar quantities of phosgene formed were very small in comparison to input concentrations of phosgene necessary to depress microsomal cytochrome P-450 and glucose-6-phosphatase. Cysteine had no statistically significant effect on covalent binding of 14CCl4 metabolites to either microsomal lipids or proteins. Furthermore, presence of cysteine had no protective effect against loss of cytochrome P-450, glucose-6-phosphatase, or the capacity of microsomes to sequester calcium ions, all of which losses occur in vitro as a result of the metabolism of either CCl4 or CBrCl3. The low level of phosgene production, the lack of any effect of cysteine on the degree of covalent binding of CCl4 metabolites, the failure of cysteine to afford any protection against CCl4- or CBrCl3-dependent loss of microsomal enzyme activity, and the relative ineffectiveness of phosgene itself as a microsomal poison argue against the possibility that formation of phosgene plays a significant role in the liver injury resulting from CCl4 or CBrCl3 intoxication. Our experiments, however, do not rule out the possibility that some phosgene production and subsequent toxicological action may occur in a hydrophobic microenvironment of the endoplasmic reticulum." @default.
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- W2037904562 title "Evaluation of a role for phosgene production in the hepatotoxic mechanism of action of carbon tetrachloride and bromotrichloromethane" @default.
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- W2037904562 doi "https://doi.org/10.1016/0041-008x(82)90282-4" @default.
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