Antigenotoxic effect of mangiferin and changes in antioxidant enzyme levels of Swiss albino mice treated with cadmium chloride

Abstract

Cadmium is an environmental metal toxin implicated in human diseases. Mangiferin (MGN), a naturally occurring glucosylxanthone, is present in Mangifera indica. In this study, the protective role of MGN against cadmium chloride (CdCl(2))-induced genotoxicity was studied in Swiss albino mice. Mice were administered with single intra-peritoneal (i.p.) optimal dose of MGN (2.5 mg/kg b.wt.) before treatment with various concentrations of CdCl(2) (7, 8, 9, 10 and 11 mg/kg b.wt.). The LD( 50(30)) was found to be 8.5 mg/kg b.wt. for DDW + CdCl(2) group, while it was increased to 9.77 mg/kg after MGN treatment resulting in increase in the LD(50(30)) value by 1.26 mg, with a dose reduction factor (DRF) of 1.14. Treatment of mice to various doses of CdCl(2) resulted in a dose-dependent increase in the frequency of micronucleated polychromatic (MnPCE) and normochromatic erythrocytes (MnNCE), with corresponding decrease in the polychromatic / normochromatic erythrocyte ratio (PCE/NCE ratio) at various post-treatment times. MGN (2.5 mg/kg b.wt.) pretreatment significantly (p < .001) reduced the frequency of MnPCE, MnNCE and increased PCE/NCE ratio when compared with the DDW + CdCl(2) group at all post-treatment times indicating its antigenotoxic effect. Further, pretreatment of MGN declined the lipid peroxidation (LPx) content in liver, whereas significant increase was observed in hepatic Glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) activity. Our study revealed that MGN has potent antigenotoxic effect against CdCl(2)-induced toxicity in mice, which may be due to the scavenging of free radicals and increased antioxidant status.