Duration of exposure modulates combined effects of arsenic and fluoride on oxidative stress in the liver of rat

Aim: Exposure time dependent combined effects of arsenic (sodium arsenate) and fluoride (sodium fluoride), two major ground water pollutants, have been studied on oxidative stress and antioxidant mechanisms in the liver of female Wistar rats. Methodology: Healthy rats were treated with sodium arsenate (4 mg kg(-1) b.wt.) and sodium fluoride (4 mg kg(-1)b.wt.) for three-time intervals, i.e., 30, 60 and 90 days through gavage. Liver tissues of exposed rats were analysed for malonaldehyde (MDA), hydrogen peroxide (H2O2), nitric oxide (NO), reduced glutathione (GSH), oxidized 2 2 glutathione (GSSG), glutathione peroxidase (GPx) and catalase (CAT). Results: Combined exposure of rats to arsenic and fluoride for selected period of exposure viz. 30, 60 and 90 days yielded different results on parameters of oxidative stress in liver. The highest values for malondialdehyde (0.610 nmoles mg(-1) protein), hydrogen peroxide (2.31 mu moles) and nitric oxide (2.57 mu moles) were recorded after 60 days of exposure. Maximum decline in GSH (0.154 mu mol g(-1) liver) after 30 days of exposure, in GSSG (110 mu mol g(-1) liver) after 90 days of exposure, GPx (1.03 nmoles NADPH min mg (-1) protein) after 30 days of exposure and catalse (74.96 units) after 30 days of exposure were registered. Results showed resistance against oxidative stress after 90 days of combined exposure to arsenic and fluoride. Interpretation: It is hypothesized that internalization of arsenic and fluoride in the hepatic parenchyma leads to the formation of a compound, arsenic trifluoride (AsF3). It was found less toxic than arsenic but more toxic than fluoride. Arsenic-protein interaction is also modulated in the presence of fluoride in the hepatic parenchymal cell.