Nickel-induced oxidative stress and effect of antioxidants in human lymphocytes.

Abstract

The purpose of this study was to evaluate the oxidative effect in human lymphocytes after acute nickel (Ni) treatment for 1 h; levels of intracellular reactive oxygen species (ROS), lipid peroxidation (LPO) and hydroxyl radicals ((*)OH) were examined in isolated lymphocytes. The potential effects of antioxidants were also examined. After acute treatment, NiCl(2) (0-10 mM) significantly decreased the viability of lymphocytes. NiCl(2) appear to increase the degree of dichlorofluorescein (DCF) fluorescence and the levels of thiobarbituric acid-reactive substances (TBARS) in human lymphocytes in vitro in a concentration-dependent manner. The level of (*)OH was quantified by two main hydroxylated derivates, 2,3- and 2,5-dihydroxybenzate (DHB). Levels of 2,3- and 2,5-DHB were significantly higher in the Ni-treated group than in controls. Catalase partially reduced the NiCl(2)-induced elevation of oxidants and TBARS, whereas superoxide dismutase (SOD) enhanced the level of oxidants and TBARS. Both NiCl(2)-induced fluorescence and LPO were prevented significantly by glutathione (GSH) and mannitol. NiCl(2)-induced increase in generation of (*)OH was prevented significantly by catalase, GSH and mannitol, but not by SOD. These results suggest that NiCl(2)-induced lymphocyte toxicity may be mediated by oxygen radical intermediates, for which the accelerated generation of (*)OH may plays an important role in Ni-induced oxidative damage of human lymphocytes. Catalase, GSH and mannitol each provides protection against the oxidative stress induced by Ni.