Evidence for the involvement of hydroxyl radicals in nickel mediated enhancement of lipid peroxidation: implications for nickel carcinogenesis.
The administration of nickel to rats resulted in enhanced hepatic lipid peroxidation, levels of glutathione and iron with a concomitant decrease in glutathione peroxidase activity. These effects were dose dependent. Enhanced lipid peroxidation was found to be inhibited by the exogenous addition of ethylenediamine tetraacetic acid (EDTA), benzoate and ethanol while catalase and superoxide dismutase were ineffective in this regard. Our data strongly suggest the involvement of hydroxyl radicals in the nickel mediated enhancement of lipid peroxidation which may have their implications in the carcinogenicity of nickel compounds.
Athar
M
M
Industrial Toxicology Research Centre, Lucknow, India.
Hasan
S K
SK
Srivastava
R C
RC
D000818:Animals; D002273:Carcinogens; D004305:Dose-Response Relationship, Drug; D005260:Female; D005609:Free Radicals; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006878:Hydroxides; D007501:Iron / Q000378:metabolism; D008054:Lipid Peroxides; D008099:Liver / Q000187:drug effects*; D009532:Nickel / Q000633:toxicity*; D051381:Rats
D002273:Carcinogens; D005609:Free Radicals; D006878:Hydroxides; D008054:Lipid Peroxides; D009532:Nickel; D007501:Iron; D005979:Glutathione Peroxidase; D005978:Glutathione