Crry receptor and oxidative stress involved in erythrocyte immune toxicity of mice caused by endosulfan and protective effects of vitamin E

The purpose of this research was to investigate if Vitamin E could decrease the toxic-effects of endosulfan on erythrocyte immunity and its regulating mechanism. The levels of endosulfan and Vitamin E were (in mg/kg/d), respectively, 0 and 0 (control group), 0.8 and 0 (endosulfan-only group), 0.8 and 100 (experimental group). The results showed that Vitamin E inhibited endosulfan-induced decreases in rosette ratios of erythrocyte C(3)b receptor and increases in rosette ratios of erythrocyte immune complex. Vitamin E reversed the decline tendency of erythrocytes to regulate T-lymphocyte activity and the increase tendency of erythrocyte immunosuppressive factor activity in plasma induced by endosulfan. Further, Vitamin E alleviated the decreases of CD35 mRNA levels in spleen and CD35 expression on B-lymphocyte surfaces, antagonized a decline in Crry mRNA levels. Lastly, Vitamin E reversed induced decreases in total anti-oxidation capability and increases in malondi-aldehyde and free radical levels in spleen caused by endosulfan. The results suggested that Vitamin E relieved endosulfan-induced effects on erythrocytes immunity, reversed changes in expression of erythrocyte immune factors, and antagonized oxidative stress. Vitamin E could stabilize the expression of Crry receptor by inhibiting oxidative stress, and thereby reverse the decrease of erythrocyte immunity caused by endosulfan.