Glutathione depletion and oxidative damage in mitochondria following exposure to cadmium in rat liver and kidney.
The dose-dependent effects of cadmium (Cd) on mitochondria and post-mitochondrial supernatant (PMS) of liver and kidney were investigated in adult male albino rats. Two groups of rats were injected intraperitoneally with 0.1 mg Cd/kg body weight and 1 mg/kg body weight, respectively, for a period of 3 months (5 days/week). This resulted in a significant decrease in total glutathione (GSH) levels, irrespective of the doses, in mitochondrial as well as in PMS fractions of liver and kidney. In contrast, end products of lipid and protein were significantly increased in a dose-dependent manner in subcellular fractions of liver and kidney. These results suggest that the depletion of tissue glutathione levels is not a primary reason of the observed oxidative damage in liver and kidney caused by Cd.
Predictive Toxicology Research Group, Industrial Toxicology Research Centre, Lucknow, India.
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Nigam
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Shukla
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Agarwal
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000032:analysis*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats
D002104:Cadmium; D005978:Glutathione