Effect of selected antioxidants in beta-cyfluthrin-induced oxidative stress in human erythrocytes in vitro.

beta-Cyfluthrin is one of the most widely used type II pyrethroid in agriculture. The aim of this study was to examine (1) the possibility of beta-cyfluthrin to induce oxidative stress in human erythrocytes in vitro and its effect on catalase (CAT) and superoxide dismutase (SOD) activities as well as (2) the role of melatonin (MEL; 2mM), its precursor--N-acetylserotonin (NAS; 1mM), quercetin (Q; 80 microM) and rutin (R; 80 microM) in alleviating the cytotoxic effects of beta-cyfluthrin. Erythrocytes were divided into portions. The first portion was incubated for 4h at 37 degrees C with different concentrations (0, 43, 215, 1075 ppm) of beta-cyfluthrin. The other portions were preincubated with selected antioxidant, respectively for 30 min and followed by beta-cyfluthrin incubation for 4h. Malondialdehyde (MDA) concentrations, CAT and SOD activities, as well as haemolysis percentage (H) were measured in all treatment portions of erythrocytes. It could be concluded that the in vitro toxicity of beta-cyfluthrin may be associated with oxidative stress. Significant reduction in the activities of CAT was observed at all beta-cyfluthrin concentrations, while SOD activities were significantly decreased only in erythrocytes incubated with the highest beta-cyfluthrin concentration. SOD activity of the non-pretreated erythrocytes exposed to the lowest dose of beta-cyfluthrin was significantly greater when compared to comparably beta-cyfluthrin-exposed antioxidant pretreated cells. The highest concentration of beta-cyfluthrin has caused over 35% haemolysis, and the lowest concentration about 15%. MEL pretreatment had no effect on H and MDA induction by beta-cyfluthrin. NAS, Q and R reduced H and MDA level, but could not prevent induction of these parameters. Compared to other antioxidants NAS appeared to maintain better the CAT activity at control levels for all doses of beta-cyfluthrin. Pretreatment with Q was found to protect against the decrease in SOD activity induced by beta-cyfluthrin.