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Environ Toxicol Pharmacol. 2017 Dec;56:99-105. doi: 10.1016/j.etap.2017.08.034. Epub 2017 Sep 1.

Lead induces apoptosis in mouse TM3 Leydig cells through the Fas/FasL death receptor pathway.

Author information

1
College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan, 450002, China.
2
College of Veterinary Medicine, Hunan Agricultural University, Changsha, Hunan, 410128, China. Electronic address: wu23jing@aliyun.com.
3
College of Veterinary Medicine, Hunan Agricultural University, Changsha, Hunan, 410128, China.
4
College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan, 450002, China. Electronic address: linfeng7207@163.com.

Abstract

The study was aimed to investigate the effect of Pb toxicity on mouse Leydig cells and its molecular mechanism. The TM3 cells were cultured in vitro and exposed to Pb at different concentrations for 24h. The effects of Pb on cell proliferation and apoptosis were analyzed with MTT and Annexin V-FITC/PI via flow cytometry, respectively. Expression levels of Fas, Fas-L and caspase-8 in TM3 cells were determined by western blot. As well as the inhibitory effect of the caspase-8 inhibitor Z-IETD-FMK on cell apoptosis. We found that Pb treatment significantly decreased the cellar viability (P<0.05), increased the apoptosis (P<0.01) and the Fas, FasL, and caspase-8 expression levels in Pb-treated cells as compared to the control cells (P<0.05 or P<0.01). Furthermore, the caspase-8 inhibitor effectively block the Pb-induced cell apoptosis. Taken together, our data suggest that Pb-induced TM3 cell toxic effect may involve in the Fas/FasL death receptor signaling pathway.

KEYWORDS:

Apoptosis; Caspase-8; Cytotoxicity; Fas/FasL; Lead; TM3 leydig cells

PMID:
28889079
DOI:
10.1016/j.etap.2017.08.034
[Indexed for MEDLINE]

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