Author(s): Hussain T, Shukla GS, Chandra SV
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Abstract Intraperitoneal administration of cadmium acetate (Cd2+, 0.4 mg/kg) to rats daily for 30 days was found to inhibit the activity of superoxide dismutase (SOD), to increase the endogenous levels of lipid peroxides and lipid peroxidation in the liver and the kidney tissues. Addition of varying concentrations of Cd2+ (10-100 microM) in vitro also inhibited SOD in both the tissues. It appears that the inhibition of SOD could be due to direct interaction of Cd2+ with the enzyme molecule. Lipid peroxidation reaction was also increased after addition of Cd2+ to fresh homogenate of these tissues, however, it did not produce any effect in heated homogenates in in vitro experiments. It indicated that Cd-induced elevation in lipid peroxidation may not be only due to the possibility of higher level of superoxide radicals resulting from inhibited superoxide dismutase but could also be as a result of direct action of Cd2+ on the peroxidation reaction. Thus, the possibility of involvement of free radical damage to the membrane structures in Cd toxicity has been demonstrated in these experiments.
This article was published in Pharmacol Toxicol
and referenced in Journal of Clinical Toxicology