No abstract

Cadmium (Cd) is a non-redox metal that can indirectly cause oxidative stress by depleting cellular levels of glutathione. It is well-known for the generating reactive oxygen species (ROS) such as hydroxyl radicals, superoxide anions, nitric oxide, and hydrogen peroxide. The latter inactivates antioxidant enzymes and induces lipid peroxidation and DNA damage in cells. In our study, we have investigated the ameliorative effect of limonene against Cd-induced genotoxicity using various biomarkers such as sister chromatid exchange (SCE), comet, and lipid peroxidation (LPA) assays in cultured human peripheral blood lymphocytes (PBL) from healthy individuals. It is a naturally occurring flavonoid, found in essential oil of citrus fruits. Limonene at 20-μM and 100-μM concentrations had significantly (P < 0.05 and P < 0.01) reduced the SCE frequency, tail moment, and peroxidation of lipids. Ameliorative effect of limonene was also determined by measuring the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT). We found a significant increase (P < 0.05) in the enzyme activity after limonene treatment. We also studied the effect of GSTP1 gene polymorphism on Cd-induced genotoxicity and antigenotoxic potential of limonene. We found a significant decrease (P < 0.05) in SCE frequency, tail moment, and lipid peroxidation after limonene treatment compared to Cd. However, we did not observe any significant relationship (P > 0.05) between GSTP1 polymorphism and Cd, limonene genotoxicity and antigenotoxicity, respectively.

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.

Arsenic exposure is one of the major health problem worldwide. It is related with various cancers and numerous other pathological effects. The present work was aimed to study the ameliorative effects of eugenol against arsenic mediated oxidative DNA damage using Sister chromatid exchanges (SCE), comet, and lipid peroxidation assays as biomarkers. For the genotyping of GSTO2, PCR RFLP method was used. The treatment with sodium arsenite showed dose dependent increase in frequency of SCE, comet tail moment (Tm), and lipid peroxidation (TBARS levels). On administration of eugenol (10 and 20 µM) significant dose dependent decrease in the number of SCE, Tm value, and TBARS levels observed in arsenic treated cultured peripheral blood lymphocytes. Nonsignificant effects of GSTO2 polymorphism perceived on arsenic genotoxicity and eugenol antigenotoxicity. The results of the present work suggest a protective role of eugenol against arsenic induced genotoxic and oxidative damage in cultured human peripheral blood lymphocytes. Practical application Arsenic contamination of groundwater is one of the leading environmental issues worldwide. Chronic exposure of arsenic cause several health problems including tumor manifestation. The results of the present study suggest the use of indigenous dietary elements, herbs, shrubs as a safer and effective preventative medicine against heavy metal induced genotoxicity and oxidative stress.

Arsenic contamination is one of the major health concerns all over the world and associated with various types of cancer and pathological effects. The production of reactive oxygen species (ROS) plays a crucial role in arsenic mediated toxicity. Several studies have shown that population constantly exposed to arsenic have substantial oxidative stress that, in turn, induces DNA damage. In the present work eugenol and anethole were investigated for their protective effect against arsenic mediated oxidative DNA damage in peripheral blood lymphocytes. Comet assay and lipid peroxidation was used as biomarker of genotoxicity and oxidative stress respectively. A dose dependent increase in tail moment and lipid peroxidation was observed when lymphocytes were treated with sodium arsenite. Treatment of arsenic (50µM) along with eugenol (20µM) and anethole (50µM) showed a significant decrease in the tail moment and lipid peroxidation in cultured peripheral blood lymphocytes. The decrease in the tail moment and lipid peroxidation was significantly higher in combined supplementation of eugenol and anethole as compared to individual administration. The results of the present study suggests ameliorative role of eugenol and anethole against arsenic induced genotoxic and oxidative damage in cultured human peripheral blood lymphocytes.