Comparison of the effects of methyl-N-butyl ketone and phenobarbital on rat liver cytochromes P-450 and the metabolism of chloroform to phosgene☆
References (29)
- et al.
Investigation of the mechanism of the potentiation of chloroform-induced hepatotoxicity and nephrotoxicity by methyl-n-butyl ketone
Toxicol. Appl. Pharmacol.
(1981) - et al.
The role of glutathione in chloroform-induced hepatotoxicity
Exp. Mol. Pathol.
(1976) Separation and purification of multiple forms of microsomal cytochrome P-450. Partial characterization of three apparent homogeneous cytochromes P-450 prepared from livers of phenobarbital and 3-methylcholanthrene-treated rats
J. Biol. Chem.
(1978)- et al.
Acute alteration of chloroform induced hepato and nephrotoxicity by Mirex and Kepone
Toxicol. Appl. Pharmacol.
(1979) - et al.
Acute alteration of chloroform-induced hepato and nephrotoxicity by n-hexane, methyl n-butyl ketone and 2,5-hexanedione
Toxicol. Appl. Pharmacol.
(1980) The influence of some aliphatic compounds on rat liver glutathione levels
Biochem. Pharmacol.
(1965)- et al.
Characterization of three forms of rabbit microsomal cytochrome P-450 by peptide mapping utilizing limited proteolysis in sodium dodecyl sulfate and analysis by gel electrophoresis
Arch. Biochem. Biophys.
(1979) - et al.
Relative effects of various chlorinated hydrocarbons on liver and kidney function in mice
Toxicol. Appl. Pharmacol.
(1966) - et al.
Evidence for phosgene formation during liver microsomal oxidation of chloroform
Biochem. Biophys. Res. Commun.
(1977) - et al.
The carbon monoxidebinding pigment of liver microsomes. I. Evidence for its hemoprotein nature
J. Biol. Chem.
(1964)
Phosgene: A metabolite of chloroform
Biochem. Biophys. Res. Commun.
Deuterium isotope effect in bioactivation and hepatotoxicity of chloroform
Life Sci.
Deuterium isotope effect in in vivo bioactivation of chloroform to phosgene
Biochem. Pharmacol.
Oxidative bioactivation of haloforms into hepatotoxins
Cited by (28)
Diallyl disulfide, an organo-sulfur compound in garlic and onion attenuates trichloromethane-induced hepatic oxidative stress, activation of NFkB and apoptosis in rats
2018, Journal of Nutrition and Intermediary MetabolismCitation Excerpt :TCM is metabolized by oxidative or reductive cytochrome P450-dependent pathways with the former being predominant [8]. In the oxidative pathway, TCM is metabolized to phosgene [9], a highly reactive electrophilic metabolite, binding covalently to cell constituents possessing nucleophilic groups, including lipids, proteins, and glutathione [9–12], causing cytotoxicity [13,14]. TCM-induced reactive oxygen species generation is one of the direct causes of hepatic injury [6,15] The generation of these species and their overwhelming effects on cells' ability to mop them cause oxidative stress and then tissue injury [16,17].
Subchronic chloroform priming protects mice from a subsequently administered lethal dose of chloroform
2006, Toxicology and Applied PharmacologyAssessment of Liver Function in the Surgical Patient
2006, Surgery of the Liver, Biliary Tract and Pancreas: Volumes 1-2, Fourth EditionDichloroacetic acid treatment increases hepatic CYP2E1 in male and female rats
1996, Toxicology and Applied PharmacologyDifferent contributions of cytochrome P450 2E1 and P450 2B1/2 to chloroform hepatotoxicity in rat
1995, Toxicology and Applied Pharmacology
- ☆
Part of this work was presented at a meeting of the American Society of Pharmacology and Experimental Therapeutics (Pharmacologist 23, 201, 1981).
- 2
Present address: Pathology Dept., Tacoma General Hospital, 315 South K St., Tacoma, Wash. 98405.