The purpose of this study was to investigate the effects of vitamin E on reproductive hormones and testis structure in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Five experimental groups of a combination of TCDD and vitamin E were designed as follows: 0 ng/kg/d and 0 mg/kg/d (control group), 100 ng/kg/d and 0 mg/kg/d (Group I), 100 ng/kg/d and 20 mg/kg/d (Group II), 100 ng/kg/d and 100 mg/kg/d (Group III), and 100 ng/kg/d and 500 mg/kg/d (Group IV) respectively. Vitamin E and TCDD were given by oral gavage for 7 weeks. The results demonstrated that TCDD decreased the levels of brain gonadotropin releasing hormone (GnRH), testis luteinizing hormone (LH) and follicle stimulating hormone (FSH), serum testosterone and testis spermatozoa number, and damaged testis structure. Vitamin E at 20 mg/kg alleviated the decrease of GnRH; vitamin E at 20, 100, and 500 mg/kg antagonized the decline of LH and FSH; vitamin E at 20 and 100 mg/kg reversed the decrease of testosterone and spermatozoa number; and vitamin E at 100 mg/kg decreased the damage of the testis structure caused by TCDD. The results indicate that vitamin E antagonizes the reproductive endocrine toxicity and alleviates the changes in testicular structure caused by TCDD.

Abstract:The study was conducted to investigate the effects of vitamin E (VE) on reproduction endocrine and ovary structures in mice acutely treated with TCDD. Twenty-four mice were divided into control groups, TCDD-treated with 30 ug/kg group, and a TCDD-treated with 30 μg/kg followed with 100 mg/kg vitamin E group. The level of progesterone and estradiol of plasma were analyzed by radio-immunity methods. The number of ova and the ovary forms were counted and observed under the microscope. The results showed that TCDD obviously decreased the level of plasma progesterone and the number of ova, changed the forms of ovaries, while 100 mg/kg VE significantly alleviated these effects caused by TCDD. TCDD and VE had no significant effects on the levels of plasma estradiol. The results indicated that VE had anti-actions on the endocritic function and a decrease in the progesterone level and the ova number in mice, caused by TCDD.