Depletion of glutathione and hepato-toxicity caused by vinyl ethers in mice.
4-Nitrophenyl vinyl ether (NPVE) and phenyl vinyl ether (PVE) administered i.p. in mice lowered hepatic non-protein sulfhydryl (NP-SH) content, but did not elevate the serum glutamate pyruvate transaminase (GPT) activity. n-Butyl vinyl ether (BVE) showed no significant effects either on the NP-SH content or on the serum GP activity. Mice pretreated with buthionine sulfoximine were sensitive to the potential toxicity of NPVE. These results showed that aryl vinyl ethers, NPVE and PVE, are more toxic than the alkyl vinyl ether, BVE, and that glutathione plays an important role on the protection of hepatic injury by reactive metabolite(s) derived from vinyl ethers.
D000410:Alanine Transaminase / Q000097:blood*; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000378:metabolism*; D004987:Ethers / Q000633:toxicity; D005978:Glutathione / Q000378:metabolism*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010084:Oxidation-Reduction; D010647:Phenyl Ethers / Q000633:toxicity*; D013438:Sulfhydryl Compounds / Q000378:metabolism; D014753:Vinyl Compounds / Q000633:toxicity*
D004987:Ethers; D010647:Phenyl Ethers; D013438:Sulfhydryl Compounds; D014753:Vinyl Compounds; C096129:n-butyl vinyl ether; C096130:phenyl vinyl ether; C047678:(4-nitrophenyl)vinyl ether; D000410:Alanine Transaminase; D005978:Glutathione