期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 314, 期 -, 页码 98-108出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2016.11.013
关键词
Bisphenol A; Endoplasmic reticulum stress; PERK/EIF2 alpha/chop pathway; Male reproductive toxicity
资金
- Program of National Natural Science Foundation of China [81030052, 81402655]
Bisphenol A (2,2-bis(4-hydroxyphenyl)propane, BPA) is ubiquitous in the environment, wildlife, and humans. Evidence from past studies suggests that BPA is associated with decreased semen quality. However, the molecular basis for the adverse effect of BPA on male reproductive toxicity remains unclear. We evaluated the effect of BPA on mouse spermatocytes GC-2 cells and adult mice, and we explored the potential mechanism of its action. The results showed that BPA inhibited cell proliferation and increased the apoptosis rate. The testes from BPA-treated mice showed fewer spermatogenic cells and sperm in the seminiferous tubules. In addition, BPA caused reactive oxygen species (ROS) accumulation. Previous study has verified that mitochondrion was the organelle affected by the BPA-triggered ROS accumulation. We found that BPA induced damage to the endoplasmic reticulum (ER) in addition to mitochondria, and most ER stress-related proteins were activated in cellular and animal models. Knocking down of the PERK/EIF2 alpha/chop pathway, one of the ER stress pathways, partially recovered the BPA-induced cell apoptosis. In addition, an ROS scavenger attenuated the expression of the PERK/EIF2 alpha/chop pathway-related proteins. Taken together, these data suggested that the ROS regulated PERK/EIF2 alpha/chop pathway played a vital role in BPA-induced male reproductive toxicity. (C) 2016 Elsevier Inc. All rights reserved.
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