Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice

自噬 细胞凋亡 氧化应激 线粒体 毒性 活性氧 化学 肺 细胞生物学 镉 药理学 生物 生物化学 医学 内科学 有机化学
作者
Xishuai Tong,Xiaohui Fu,YU Gengsheng,Huayi Qu,Hui Zou,Ruilong Song,Yonggang Ma,Yan Yuan,Jianchun Bian,Jianhong Gu,Zongping Liu
出处
期刊:Environmental Toxicology [Wiley]
卷期号:38 (8): 1775-1785 被引量:5
标识
DOI:10.1002/tox.23804
摘要

Cadmium (Cd) is an environmental heavy metal, and its accumulation is harmful to animal and human health. The cytotoxicity of Cd includes oxidative stress, apoptosis, and mitochondrial histopathological changes. Furthermore, polystyrene (PS) is a kind of microplastic piece derived from biotic and abiotic weathering courses, and has toxicity in various aspects. However, the potential mechanism of action of Cd co-treated with PS is still poorly unclear. The objective of this study was to investigate the effects of PS on Cd-induced histopathological injury of mitochondria in the lung of mice. In this study, the results have showed that Cd could induce the activity of oxidative enzymes of the lung cells in mice, increasing the content of partial microelement and the phosphorylation of inflammatory factor NF-κB p65. Cd further destroys the integrity of mitochondria by increasing the expression of apoptotic protein and blocking the autophagy. In addition, PS solely group aggravated the lung damage in mice, especially mitochondrial toxicity, and played a synergistic effect with Cd in lung injury. However, how PS can augment mitochondrial damage and synergism with Cd in lung of mice requiring further exploration. Therefore, PS was able to exacerbate Cd-induced mitochondrial damage to the lung in mice by blocking autophagy, and was associated with the apoptosis.
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