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作者

Yingwen Mu, Jiayin Sun, Ziyuan Li, Wanxin Zhang, Zuodong Liu, Chao Li, Cheng Peng, Guanqun Cui, Hua Shao, Zhongjun Du

作者单位

Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Ji'nan, 250062, Shandong, People's Republic of China. Electronic address: chinashaohua5888@16 Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Ji'nan, 250062, Shandong, People's Republic of China. Department of Respiratory Medicine, Qilu Children's Hospital of Shandong University, 250022, Ji'nan, Shandong Province, People's Republic of China. Electronic address: cuiguanqun1000@16 Affiliations Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Ji'nan, 250062, Shandong, People's Republic of China Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Ji'nan, 250062, Shandong, People's Republic of China. Electronic address: duzj1981@16 com. Queensland Alliance for Environmental Health Sciences (QAEHS), The University of Queensland, 4108, Brisbane, Queensland, Australia.

刊名

Chemosphere

年份

2021

页码

132944

ISSN

1879-1298

关键词

Cell death Hepatotoxicity Mechanism Microplastics.

摘要

Microplastics are new environmental pollutants and have received widespread attention in recent years, but the toxicity of the MPs remains to be fully elucidated. To explore the effect of MPs on hepatotoxicity in mice and unravel the mechanism of pyroptosis and ferroptosis in the process of liver injury, we treated mice with 5.0 μm polypropylene microplastics at 0.1, 0.5 and 1 mg/mL for 4 weeks. Results revealed that MPs could damage liver structure and function with broken and reduced mitocho...更多

Microplastics are new environmental pollutants and have received widespread attention in recent years, but the toxicity of the MPs remains to be fully elucidated. To explore the effect of MPs on hepatotoxicity in mice and unravel the mechanism of pyroptosis and ferroptosis in the process of liver injury, we treated mice with 5.0 μm polypropylene microplastics at 0.1, 0.5 and 1 mg/mL for 4 weeks. Results revealed that MPs could damage liver structure and function with broken and reduced mitochondrial cristae, as well as increased levels of aspartate minotransferase , alanine aminotransferase , AST/ALT, alkaline phosphatase and lactate dehydrogenase . Treatment with MPs resulted in pyroptosis as evidenced by increasing expressions of interleukin IL-1β, IL-18. Additionally, MPs were shown to induce the NOD-like receptor protein 3 inflammasomes and apoptosis associated speck-like protein containing a caspase recruitment domain activation in liver tissue, enabling activation of Caspase-1-dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In addition, the increase of malondialdehyde and decrease of glutathione and superoxide dismutase in the liver indicated that MPs could induce oxidative damage. Moreover, MPs induced lipid peroxidation in the liver of mice could activate the expression of ferroptosis related proteins, including iron metabolism, such as transferrin receptor was active but ferritin heavy chain 1 was inhibited; amino acid metabolism, such as XCT system and glutathione peroxidase 4 were inhibited; lipid metabolism, such as acyl-CoA synthetase long-chain family member 4 was inhibited. Collectively, these findings evidenced that pyroptosis and ferroptosis occurred in MPs-induced liver injury accompanied by intense oxidative stress and inflammation.收起

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期刊