Journal ArticleDOI
Phosgene: a metabolite of chloroform.
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TLDR
It is suggested that the CH bond of CHCl3 is oxidized by a cytochrome P-450 monooxygenase to produce trichloromethanol, which spontaneously dehydrochlorinates to yield the toxic agent phosgene.About:
This article is published in Biochemical and Biophysical Research Communications.The article was published on 1977-12-07. It has received 202 citations till now. The article focuses on the topics: Phosgene & Chloroform.read more
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Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model.
TL;DR: CCl4 activates tumor necrosis factor (TNF)alpha, nitric oxide (NO), and transforming growth factors (TGF)-alpha and -beta in the cell, processes that appear to direct the cell primarily toward (self-)destruction or fibrosis.
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Properties of acyl glucuronides: implications for studies of the pharmacokinetics and metabolism of acidic drugs.
TL;DR: In this article, the properties of acyclic glucuronides were investigated for studies of the pharmacokinetics and metabolic properties of acidic drugs, and the implications of these properties for the study of drugs were discussed.
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Product toxicity and cometabolic competitive inhibition modeling of chloroform and trichloroethylene transformation by methanotrophic resting cells.
TL;DR: Significantly diminished formate oxidation by cells exposed to either CR or TCE without acetylene compared with that with acetylene suggests that the solvents themselves were not toxic under the experimental conditions but their transformation products were, suggesting a greater toxicity from CF transformation.
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Development of a physiologically based pharmacokinetic model for chloroform.
Richard A. Corley,Alan L. Mendrala,F.A. Smith,D.A. Staats,Michael L. Gargas,Rory B. Conolly,Melvin E. Andersen,Richard H. Reitz +7 more
TL;DR: The metabolic activation of chloroform to toxic intermediates was shown to occur most rapidly in the mouse, less rapid in the rat, and most slowly in humans, consistent with previous reports.
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Metabolism and lipoperoxidative activity of trichloroacetate and dichloroacetate in rats and mice
TL;DR: DCA was found to be the more potent of the chlorinated acetates in increasing TBARS formation in the livers of both rats and mice and enhanced the formation of TBARS in a dose-dependent manner, thereby providing further evidence of a reductive metabolic pathway.
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Relative effects of various chlorinated hydrocarbons on liver and kidney function in mice.
TL;DR: In this article, the median effective doses for inducing hepatic dysfunction were calculated and compared to the lethal doses of 1,1,2-trichloroethane and carbon tetrachloride.
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Bioactivation of carbon tetrachloride, chloroform and bromotrichloromethane: role of cytochrome P-450.
TL;DR: It is concluded that cytochrome P-450 is the site of bioactivation of these three compounds rather than NADPH cy tochrome c reductase and that CCl4 bioactivation proceeds by cyto Chrome P- 450 dependent reductive pathways, while CHCl3 activation proceeds by CytochromeP-450 dependent oxidative pathways.
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Chloroform toxicity in mice: Correlation of renal and hepatic necrosis with covalent binding of metabolites to tissue macromolecules
TL;DR: Results suggest that the covalent binding is due to a metabolite of CHCl 3, which is causally related to the tissue necrosis and obtained from autoradiograms showing that the radioactivity is located mainly in the necrotic lesions.
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Induction of Hepatomas in Mice by Repeated Oral Administration of Chloroform, with Observations on Sex Differences
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Mechanisms of Acute Hepatic ToxicityChloroform, Halothane, and Glutathione
TL;DR: Hepatotoxicity of chloroform appears to be related to two factors: 1) rate of biotransformation; 2) availability of the hepatic antioxidant, CSH.