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

Author:

Tong Xishuai123ORCID,Fu Xiaohui123,Yu Gengsheng123,Qu Huayi123,Zou Hui123,Song Ruilong123,Ma Yonggang123,Yuan Yan123ORCID,Bian Jianchun123ORCID,Gu Jianhong123ORCID,Liu Zongping123ORCID

Affiliation:

1. Institutes of Agricultural Science and Technology Development (Joint International Research laboratory of Agriculture and Agri‐Product Safety of the Ministry of Education of China)/College of Veterinary Medicine Yangzhou University Yangzhou 225009 China

2. Jiangsu Co‐innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses Yangzhou 225009 China

3. Jiangsu Key Laboratory of Zoonosis Yangzhou 225009 China

Abstract

AbstractCadmium (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.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Jiangsu Province

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

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