Influence of cadmium intoxication on hepatic lipid peroxidation, glutathione level, and glutathione S-transferase and gamma-glutamyl transpeptidase activities: correlation with chromosome aberrations in bone marrow cells.

We examined whether there was any correlation between chromosome aberrations (CAs) in bone marrow cells with hepatic lipid peroxidation (LPO), reduced glutathione (GSH) level, glutathione S-transferase (GST), and gamma-glutamyl transpeptidase (GGT) activity after cadmium (Cd) intoxication in both a dose- and a time-dependent manner. Cadmium chloride was administered subcutaneously in doses of 0.5, 1.5, 2.5, and 5.0 mg/kg body weight to Swiss albino Balb/c male mice. The animals were exposed for 8, 16, and 24 days, i.e., 4, 8, and 12 doses, respectively. Biochemical parameters were measured in hepatic tissue for a correlation with chromosome aberrations in bone marrow. With the increment of dose and advancement of time points, the biochemical, as well as the cytogenetic, parameters altered significantly. Hepatic lipid peroxidation and GGT activity increased significantly along with an increased percentage of chromosome aberrations in the bone marrow, but the hepatic reduced glutathione level and GST activity were found to decrease following Cd administration. Up to 5.0 mg Cd/kg body weight, lipid peroxidation did not exhibit threshold levels of toxicity as shown by the two-way (fixed effect) analysis of variance test. In contrast, the observed values of reduced glutathione levels, GST and GGT activity, and chromosome aberrations in bone marrow showed threshold activity levels. Therefore, there might be a relationship between an increase in the frequency of chromosome aberrations, elevated lipid peroxidation, and depleted glutathione levels and GST and GGT activity. The clastogenic efficacy of Cd may be mediated through the biochemical pathways.