title: Crry receptor and oxidative stress involved in erythrocyte immune toxicity of mice caused by endosulfan and protective effects of vitamin E.
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 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.
authors.affiliation: Department of Microbiology, School of Basic Medical Sciences, Capital Medical University, China.
authors.forename: Yan-Hua
authors.initials: YH
authors.lastname: Wu
authors.forename: Jing
authors.initials: J
authors.lastname: Jia
authors.forename: Yan-Bo
authors.initials: YB
authors.lastname: Li
authors.forename: Zhi-Xiong
authors.initials: ZX
authors.lastname: Shi
authors.forename: Xian-Qing
authors.initials: XQ
authors.lastname: Zhou
authors.forename: Zhi-Wei
authors.initials: ZW
authors.lastname: Sun
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D004726:Endosulfan / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D004912:Erythrocytes / Q000276:immunology*; D007306:Insecticides / Q000633:toxicity*; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D011951:Receptors, Complement / Q000235:genetics / Q000378:metabolism*; D017463:Receptors, Complement 3b / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D012397:Rosette Formation; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; C081470:Cr1l protein, mouse; D007306:Insecticides; D012333:RNA, Messenger; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D014810:Vitamin E; D004726:Endosulfan