The Journal of Toxicological Sciences
Online ISSN : 1880-3989
Print ISSN : 0388-1350
ISSN-L : 0388-1350
Original Article
Crry receptor and oxidative stress involved in erythrocyte immune toxicity of mice caused by endosulfan and protective effects of vitamin E
Yan-Hua WuJing JiaYan-Bo LiZhi-Xiong ShiXian-Qing ZhouZhi-Wei Sun
Author information
JOURNALS FREE ACCESS

2012 Volume 37 Issue 6 Pages 1225-1237

Details
Abstract

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 C3b 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.

Information related to the author
© 2012 The Japanese Society of Toxicology
Previous article Next article
feedback
Top