The protective effects of vitamin E (45, 150, and 500 mg/kg/d) against reproductive toxicity induced in male Kunming mice by intragastric administration of 120 mg/kg/d bisphenol A was investigated. After two weeks, relative organ weights, sperm counts, sperm abnormality rates and serum testosterone concentrations were determined. Epididymal sperm counts were significantly decreased, sperm abnormality was increased, and serum testosterone concentrations were dramatically reduced following bisphenol A exposure. Vitamin E treatment led to a marked increase in sperm numbers and a decrease in the proportion of malformed sperm in a dose-related manner; serum testosterone levels were also restored. This suggests that vitamin E could be used as prophylactic agent for preventing bisphenol A-induced reproductive toxicity.
Ma Lin,Yu Haiyang,Wang Xu,Li Dan,Zhang Yumin,Pei Xiucong,Duan Zhiwen,Ma Mingyue
The effect of prenatal bisphenol A (BPA) exposure is increasingly concerned. We investigated the effect of maternal BPA exposure during pregnancy on male offspring and its potential mechanism. Thirty pregnant Sprague Dawley (SD) rats were randomly divided into exposed and control groups. At PND56, the number of sperm, luteinizing hormone, and testosterone in the BPA-exposed group decreased, and testicular tissue structure was damaged in offsprings. At GD20, the miRNA profile in the testis of male offspring was examined and the expression levels of 28 deregulated miRNAs were validated by qRT-PCR. We found that miR-361-5p , miR-203a-3p , and miR-19b-2-5p had significantly different expression levels in the testis. These results suggest that maternal exposure to BPA can lead to differential changes in progeny miRNAs, which will provide direction for future in-depth mechanisms of reproductive injury.
Jiang Zhihui,Zhou Bo,Li Xinping,Kirby Gordon M.,Zhang Xiaoying
Male infertility is a major health issue with an estimated prevalence of 4.2% of male infertility worldwide. Our early work demonstrated that Cistanche extracts protect against sperm damage in mice and that echinacoside (ECH) is one of the major active components. Here we report an essential role for ECH, a natural product that reverses or protects against oligoasthenospermia in rats. ECH was assayed by HPLC, the quantity and quality of sperm was evaluated and hormone levels were determined by radioimmunosorbent assay. ECH reduced levels of androgen receptor (AR) and key steroidogenic-related genes as determined by Western blot and qPCR analysis. The interaction between ECH and AR were evaluated by indirect ELISA and molecular docking. The results show that ECH combined with hypothalamic AR in the pocket of Met-894 and Val-713 to inhibit transfer of AR from the cytoplasm to nuclei in the hypothalamus. While negative feedback of sex hormone regulation was inhibited, positive feedback was stimulated to increase the secretion of luteinizing hormone and testosterone subsequently enhancing the quantity of sperm. Taken together, these data demonstrate that ECH blocks AR activity in the hypothalamus to increase the quantity of sperm and protect against oligoasthenospermia in rats.
危险品化学品经营许可证（带存储）