State Key Lab of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing 210029, PR China.
Toxicol Lett. 2013 May 23;219(2):116-24. doi: 10.1016/j.toxlet.2013.03.011. Epub 2013 Mar 22.
To investigate the effects of a low bisphenol A (BPA) concentration on male reproduction, adult rats were administered a concentration of BPA that was less than the no observable adverse effect level (0.0005-5 mg/kg/bw) for 8 weeks. General toxicity, reproductive hormones, and spermatogenesis were then determined. The expression of genes related to hormone synthesis and spermatogenesis was also analyzed. These BPA concentrations generated no general toxicity and no significant changes on serum hormones. However, the testicular testosterone, hormone synthesis-related genes StAR and Cyp450scc increased, whereas 3β-HSD, 17β-HSD, and Cyp450arom decreased. Additionally, BPA significantly decreased the epithelial height and round spermatids in seminiferous tubules, sperm count, androgen receptor expression, and the expression of the spermatogenesis-related genes outer dense fiber protein 1 (ODF1) and transition protein 1. Our results indicate that a low BPA concentration can induce spermatogenesis disorders mainly through decreasing androgen receptor expression. The present results may bring attention to the risk of environmental BPA exposure.
为了研究低浓度双酚 A(BPA)对男性生殖的影响,将成年大鼠给予低于无观察不良效应水平(0.0005-5mg/kg/bw)的 BPA 浓度 8 周。然后测定一般毒性、生殖激素和精子发生情况。还分析了与激素合成和精子发生相关的基因的表达。这些 BPA 浓度没有产生一般毒性,也没有对血清激素产生显著影响。然而,睾丸睾酮、激素合成相关基因 StAR 和 Cyp450scc 增加,而 3β-HSD、17β-HSD 和 Cyp450arom 减少。此外,BPA 还显著降低了曲细精管上皮细胞的高度和圆形精子细胞、精子计数、雄激素受体表达以及精子发生相关基因外致密纤维蛋白 1(ODF1)和转换蛋白 1 的表达。我们的结果表明,低浓度 BPA 主要通过降低雄激素受体表达来诱导精子发生障碍。本研究结果可能会引起人们对环境 BPA 暴露风险的关注。