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二氧化硅纳米颗粒诱导精母细胞中未折叠蛋白反应介导的细胞凋亡。

Silica nanoparticles induce unfolded protein reaction mediated apoptosis in spermatocyte cells.

作者信息

Ren Lihua, Liu Jianhui, Wei Jialiu, Du Yefan, Zou Kaiyue, Yan Yongyang, Wang Zhihao, Zhang Linruo, Zhang Tong, Lu Hong, Zhou Xianqing, Sun Zhiwei

机构信息

Division of Maternal and Child Nursing, School of Nursing, Peking University Health Science Centre, No 38 Xueyuan Road, Haidian District, Beijing 100191, China.

Department of Toxicology and Hygienic Chemistry, School of Public Health, Capital Medical University, No 10 Xi Tou Tiao, Fengtai District, Beijing 100069, China.

出版信息

Toxicol Res (Camb). 2020 Jul 3;9(4):454-460. doi: 10.1093/toxres/tfaa036. eCollection 2020 Jul.

Abstract

With increasing air pollution, silica nanoparticles (SiNPs), as a main inorganic member of PM, have gained increasing attention to its reproductive toxicity. Most existing studies focused on the acute exposure, while data regarding the chronic effect of SiNPs on reproduction is limited. Therefore, this study was designed to evaluate the chronic toxicity of SiNPs on spermatocyte cells. The cells were continuously exposed to SiNPs for 1, 10, 20 and 30 generations at dose of 5 μg/ml SiNPs for 24 h per generation after attachment. The results showed that with the increasing generations of the exposure, SiNPs decreased the viability of spermatocyte cells, induced apoptosis and increased the level of reactive oxygen species in spermatocyte cells. Moreover, SiNPs increased the protein expression of GRP-78, p-PERK, IRE1α, ATF6 and Cleaved caspase-3 in spermatocyte cells, suggesting that SiNPs improved unfolded protein response (UPR) and apoptosis. The present results indicated that the long-term and low-dose exposure to SiNPs could induce apoptosis by triggering ROS-mediated UPR in spermatocyte cells.

摘要

随着空气污染的加剧,作为颗粒物主要无机成分的二氧化硅纳米颗粒(SiNPs),其生殖毒性越来越受到关注。大多数现有研究集中在急性暴露方面,而关于SiNPs对生殖的慢性影响的数据有限。因此,本研究旨在评估SiNPs对精母细胞的慢性毒性。细胞贴壁后,以5μg/ml SiNPs的剂量连续暴露于SiNPs 1、10、20和30代,每代暴露24小时。结果表明,随着暴露代数的增加,SiNPs降低了精母细胞的活力,诱导了细胞凋亡,并增加了精母细胞中的活性氧水平。此外,SiNPs增加了精母细胞中GRP-78、p-PERK、IRE1α、ATF6和Cleaved caspase-3的蛋白表达,表明SiNPs促进了未折叠蛋白反应(UPR)和细胞凋亡。目前的结果表明,长期低剂量暴露于SiNPs可通过触发精母细胞中ROS介导的UPR诱导细胞凋亡。

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