NAC通过抑制内质网应激保护镉诱导的睾丸生殖细胞凋亡

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Bibliographic Details
Published in亚洲男性学杂志：英文版 no. 2; pp. 290 - 296
Main Author Yan-Li Ji Hua Wang Cheng Zhang Ying Zhang Mei Zhao Yuan-Hua Chen De-Xiang Xu
Format Journal Article
LanguageEnglish
Published 2013
Subjects
NAC
内质网应激
凋亡
睾丸
镉
非折叠蛋白反应
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Bibliography:31-1795/R
antioxidant; apoptosis; cadmium; endoplasmic reticulum stress; N-acetylcysteine （NAC）; testis; unfolded protein response
Cadmium （Cd） is a reproductive toxicant that induces germ cell apoptosis in the testes. Previous studies have demonstrated that endoplasmic reticulum （ER） stress is involved in Cd-induced germ cell apoptosis. The aim of the present study was to investigate the effects of N-acetylcysteine （NAC）, an antioxidant, on Cd-induced ER stress and germ cell apoptosis in the testes. Male CD-1 mice were intraperitoneally injected with CdCl2 （2.0 mg kg^-1）. As expected, acute Cd exposure induced germ cell apoptosis in the testes, as determined by terminal dUTP nick-end labelling （TUNEL）. However, the administration of NAC alleviated Cd-induced germ ceil apoptosis in the testes. Further analysis showed that NAC attenuated the Cd-induced upregulation of testicular glucose-regulated protein 78 （GRP78）, an important ER molecular chaperone. Moreover, NAC inhibited the Cd-induced phosphorylation of testicular eukaryotic translation initiation factor 2a （elF2a）, a downstream target of the double-stranded RNA-activated kinase-like ER kinase （PERK） pathway. In addition, NAC blocked the Cd-induced activation of testicular X binding protein （XBP）-1, indicating that NAC attenuates the Cd-induced ER stress and the unfolded protein response （UPR）. Interestingly, NAC almost completely prevented the Cd-induced elevation of C/EBP homologous protein （CHOP） and phosphorylation of c-Jun N-terminal kinase （.INK）, two components of the ER stress-mediated apoptotic pathway. In conclusion, NAC protects against Cd-induced germ cell apoptosis by inhibiting endoplasmic reticulum stress in the testes.
ISSN:1008-682X
1745-7262