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

β-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 β-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; 2 mM), its precursor – N-acetylserotonin (NAS; 1 mM), quercetin (Q; 80 μM) and rutin (R; 80 μM) in alleviating the cytotoxic effects of β-cyfluthrin. Erythrocytes were divided into portions. The first portion was incubated for 4 h at 37 °C with different concentrations (0, 43, 215, 1075 ppm) of β-cyfluthrin. The other portions were preincubated with selected antioxidant, respectively for 30 min and followed by β-cyfluthrin incubation for 4 h. 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 β-cyfluthrin may be associated with oxidative stress. Significant reduction in the activities of CAT was observed at all β-cyfluthrin concentrations, while SOD activities were significantly decreased only in erythrocytes incubated with the highest β-cyfluthrin concentration. SOD activity of the non-pretreated erythrocytes exposed to the lowest dose of β-cyfluthrin was significantly greater when compared to comparably β-cyfluthrin-exposed antioxidant pretreated cells. The highest concentration of β-cyfluthrin has caused over 35% haemolysis, and the lowest concentration about 15%. MEL pretreatment had no effect on H and MDA induction by β-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 β-cyfluthrin. Pretreatment with Q was found to protect against the decrease in SOD activity induced by β-cyfluthrin.