MOE Key Lab of Environment and Health, Department of Occupational and Environmental Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, Hubei, China.
Hanyang Center for Disease Control and Prevention, Wuhan, Hubei, China.
Environ Toxicol. 2017 Mar;32(3):1007-1023. doi: 10.1002/tox.22300. Epub 2016 Jun 14.
Bisphenol A (BPA) exposure is ubiquitous, and in laboratory animals and humans, exposure has been associated with male spermatogenesis dysfunction. However, it is largely unknown if this association has a fetal origin.
The aim of this research is to explore the mechanism whereby prenatal BPA exposure exerts its reproductive toxicities on spermatogenesis in male offspring.
We fed pregnant SD rats BPA at doses ranging from 1 to 100 mg/kg body weight during gestation days 14-21. The male offspring were euthanized at postnatal day 21, and the levels of sex hormones and reactive oxygen species (ROS), expressions of proteins and genes in the Akt/mTOR, and mitochondrial apoptosis pathways were detected. Several closely linked autophagy indexes were also measured incidentally. Additionally, semen quality of adult offspring was tested at the end of the study.
The results revealed that prenatal BPA exposure can cause endocrine disruption and oxidative stress in male offspring, leading to inhibition of spermatogenesis by suppressing the Akt/mTOR pathway and activating the mitochondrial apoptosis pathway.
These preliminary results indicate noteworthy and far-reaching effects of BPA on the reproductive system of male offspring. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1007-1023, 2017.
双酚 A（BPA）的暴露无处不在，在实验动物和人类中，暴露与男性精子发生功能障碍有关。然而，目前还不清楚这种关联是否具有胎儿起源。
本研究旨在探讨产前 BPA 暴露对雄性后代精子发生产生生殖毒性的机制。
我们在妊娠第 14-21 天给 SD 大鼠喂食 BPA，剂量范围为 1-100mg/kg 体重。雄性后代在出生后第 21 天被安乐死，并检测性激素和活性氧（ROS）水平、Akt/mTOR 和线粒体凋亡途径中的蛋白质和基因表达。还意外地测量了几个密切相关的自噬指标。此外，在研究结束时还测试了成年后代的精液质量。
结果表明，产前 BPA 暴露可导致雄性后代内分泌失调和氧化应激，通过抑制 Akt/mTOR 途径和激活线粒体凋亡途径抑制精子发生。
这些初步结果表明 BPA 对雄性后代生殖系统具有显著且深远的影响。© 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1007-1023, 2017.
