Antimony trichloride induces a loss of cell viability via reactive oxygen species-dependent autophagy in A549 cells

被引:34
作者
Zhao, Xinyuan [1 ]
Xing, Fengjun [1 ]
Cong, Yewen [1 ]
Zhuang, Yin [1 ]
Han, Muxi [1 ]
Wu, Zhiqiang [1 ]
Yu, Shali [1 ]
Wei, Haiyan [1 ]
Wang, Xiaoke [1 ]
Chen, Gang [1 ]
机构
[1] Nantong Univ, Sch Publ Hlth, Dept Occupat Med & Environm Toxicol, Nantong 226019, Peoples R China
基金
中国国家自然科学基金;
关键词
Antimony; Autophagy; Pulmonary toxicity; ROS; Cell viability loss; MICROGLIA INFLAMMATORY RESPONSE; OXIDATIVE STRESS; PROTECTIVE ROLE; ACTIVATION; APOPTOSIS; INDUCTION; MTOR; LC3; PNEUMOCONIOSIS; AGGREGATION;
D O I
10.1016/j.biocel.2017.10.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Antimony (Sb) is one of the most prevalent heavy metals and frequently leads to biological toxicity. Although autophagy is believed to be involved in metal-associated cytotoxicity, there is no evidence of its involvement following exposure. Moreover, the underlying mechanism of autophagy remains unclear. In this study, treatment with antimony trichloride caused autophagy in a dose- and time-dependent manner in A549 cells but did not affect the level of Atg5 or Atg7 mRNA expression. Furthermore, Sb enhanced autophagic flux while upregulating p62 gene and protein levels. The classic mechanistic target of rapamycin (mTOR) pathway is not involved in Sb-induced autophagy. However, Sb-induced autophagy and the upregulation of p62 were inhibited by treatment with the antioxidant N-acetylcysteine (NAC). Subsequent analyses demonstrated that the inhibition of autophagy protected A549 cells from a loss of cell viability, while the activation of autophagy by rapamycin had the opposite effect. These data suggest that reactive oxygen species-dependent autophagy mediates Sb-stimulated cell viability loss in A549 cells.
引用
收藏
页码:32 / 40
页数:9
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