Journal
ENVIRONMENTAL TOXICOLOGY
Volume 32, Issue 8, Pages 1977-1989Publisher
WILEY
DOI: 10.1002/tox.22339
Keywords
bisphenol A; autophagy; apoptosis; testis; spermatogenesis
Categories
Funding
- National Natural Science Foundation of China [81172623, 81372960]
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Bisphenol A (BPA), a typical endocrine disrupting chemical (EDC), has been proven to cause male reproductive toxicity. However, the precise mechanisms of this effect are still unclear. Puberty is a crucial period of reproductive development, and adolescents are more susceptible to xenobiotics. This research was designed to explore the mechanism of BPA toxicity on pubertal male reproduction. Rats were exposed to 0, 2, 10, 50 mg kg(-1) bw BPA, then the levels of sex hormones, oxidative stress, and semen quality were detected. HE staining, TUNEL assay and transmission electron microscopy were used to investigate the morphological changes, apoptosis, and autophagy in testes, respectively. Expressions of relevant genes and proteins were measured by RT-PCR, western blotting, and immunohistochemical staining. The results indicated that BPA exposure led to oxidative stress and endocrine disorders in pubertal male SD rats, caused apoptosis and autophagy in testes, and then damaged spermatogenesis ultimately. The Akt pathway was activated and the mTOR pathway was inhibited in the process. Taken together, BPA induced apoptosis and autophagy concurrently in pubertal testes, and this added a new layer to our understanding on male reproductive toxicity of BPA. (C) 2016 Wiley Periodicals, Inc.
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