Abstract：
:Inorganic arsenic (iAs), a ubiquitous element and a natural drinking water contaminant, has been found to impair male reproductive function. However, the effect of long-term exposure to arsenic on testis damage and its underlying mechanisms still require further evaluation. In the study, male C57BL/6 mice (4 weeks) were treated with sodium arsenite at the doses of 5 or 50 ppm arsenic via drinking water for 180 days. Sperm count, histology in testes, oxidative stress biomarkers, cell cycle progress and apoptosis were assessed. Our results showed that arsenite seriously destroyed the structure of the testes and reduced the sperm count. Arsenite significantly decreased the activity of total superoxide dismutase (T-SOD) and glutathione (GSH) content but increased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in testes. Furthermore, arsenite could induce G2/M phase arrest in testes, concurrent with a significant decrease in mRNA and protein levels of cdc2 and cyclin B1, the upregulation of p-cdc2, and an increase in mRNA levels of p53 and p21. Arsenite induced testicular apoptosis with a significant increase in Bax mRNA and protein levels, especially the caspase-3 activation. Testicular toxicity of the high dose group was stronger than that of the low dose group. In conclusion, testicular toxicity due to long-term exposure to arsenite may relate to oxidative damage, G2/M arrest and promoted apoptosis in the testes of mice, which contributed to the increased risk of spermatogenesis disorders and male infertility.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Zeng Q,Yi H,Huang L,An Q,Wang Hdoi
10.1016/j.tox.2018.09.010subject
Has Abstractpub_date
2019-01-01 00:00:00pages
122-132eissn
0300-483Xissn
1879-3185pii
S0300-483X(18)30396-2journal_volume
411pub_type
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