Shielding effect of anethole against arsenic induced genotoxicity in cultured human peripheral blood lymphocytes and effect of GSTO1 polymorphism.

Chronic exposure of inorganic arsenic compounds is responsible for the manifestation of various tumours as well as other diseases. The principal mechanism behind arsenic toxicity is the induction of a strong oxidative stress with production of free radicals in cells. The present study was aimed to explore the shielding effect of anethole against oxidative damage induced by arsenic in cultured human peripheral blood lymphocytes and the effect of GSTO1 polymorphism. Sister chromatid exchange (SCE) frequency, comet tail moment and lipid peroxidation levels were used as biomarkers to assess the oxidative damage. Heparinised venous blood was collected from healthy individuals and treated with sodium arsenite (50 µM) in the presence of anethole (25 and 50 µM) for the analysis of shielding effect of anethole. For the genotyping of GSTO1, PCR RFLP method was adopted. A significant dose-dependent increase in the frequency of SCEs, tail moment and lipid peroxidation levels, was observed when lymphocytes were treated with sodium arsenite. Anethole in combination with sodium arsenite has shown a dose-dependent significant decrease in the frequency of SCEs, tail moment and lipid peroxidation levels. Genetic polymorphism of GSTO1 was found to effect individual susceptibility towards arsenic-mediated genotoxicity and was found insignificant when antigenotoxic effect of anethole was considered. GSTO1 mutant genotypes were found to have significant higher genotoxicity of sodium arsenite as compared to wild-type genotype. The results of the present study suggest ameliorative effects of anethole against arsenic-mediated genotoxic damage in cultured human peripheral blood lymphocytes. A significant effect of GSTO1 polymorphism was observed on genotoxicity of sodium arsenite.