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聚苯乙烯微塑料通过PTEN/PI3K/AKT/mTOR诱导鸟类肺部自噬和凋亡。

Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR.

作者信息

Lu Hongmin, Yin Kai, Su Heng, Wang Dongxu, Zhang Yue, Hou Lulu, Li Jun Bo, Wang Yu, Xing Mingwei

机构信息

College of Wildlife and Protected Area, Northeast Forestry University, Harbin, People's Republic of China.

College of Resources and Environment, Northeast Agricultural University, Harbin, People's Republic of China.

出版信息

Environ Toxicol. 2023 Jan;38(1):78-89. doi: 10.1002/tox.23663. Epub 2022 Oct 7.

DOI:10.1002/tox.23663
PMID:36205374
Abstract

Microplastics (MPs) seriously pollute and potentially threaten human health. Birds are sentinels of environmental pollutants, which respond quickly to contamination events and reveal current environmental exposure. Therefore, birds are good bioindicators for monitoring environmental pollutants. However, the mechanism of lung injury in birds and the role of the PTEN/PI3K/AKT axis are unknown. In this study, broilers treated with different polystyrene microplastics (PS-MPs) (0, 1, 10, and 100 mg/L) were exposed to drinking water for 6 weeks to analyze the effect of PS-MPs on lung injury of broilers. The results showed that with the increase of PS-MPs concentration, malonaldehyde (MDA) content increased, and catalase (CAT) and glutathione (GSH) activity decreased, further leading to oxidative stress. PS-MPs caused the PI3K/Akt/mTOR pathway to be inhibited by phosphorylation, and autophagy accelerated formation (LC3) and degradation (p62), causing autophagy. In PS-MPs exposed lung tissues, the expression of Bax/Bcl-2 and Caspase family increased, and MAPK signaling pathways (p38, ERK, and JNK) showed an increase in phosphorylation level, thus leading to cell apoptosis. Our research showed that PS-MPs could activate the antioxidant system. The antioxidant system unbalance-regulated Caspase family, and PTEN/PI3K/AKT pathways initiated apoptosis and autophagy, which in turn led to lung tissue damage in chickens. These results are of great significance to the toxicological study of PS-MPs and the protection of the ecosystem.

摘要

微塑料(MPs)严重污染并可能威胁人类健康。鸟类是环境污染物的哨兵,它们对污染事件反应迅速并揭示当前的环境暴露情况。因此,鸟类是监测环境污染物的良好生物指示物。然而,鸟类肺损伤的机制以及PTEN/PI3K/AKT轴的作用尚不清楚。在本研究中,将不同浓度(0、1、10和100 mg/L)的聚苯乙烯微塑料(PS-MPs)处理的肉鸡通过饮用水暴露6周,以分析PS-MPs对肉鸡肺损伤的影响。结果表明,随着PS-MPs浓度的增加,丙二醛(MDA)含量增加,过氧化氢酶(CAT)和谷胱甘肽(GSH)活性降低,进一步导致氧化应激。PS-MPs导致PI3K/Akt/mTOR通路因磷酸化而受到抑制,自噬加速形成(LC3)和降解(p62),引发自噬。在暴露于PS-MPs的肺组织中,Bax/Bcl-2和半胱天冬酶家族的表达增加,丝裂原活化蛋白激酶信号通路(p38、ERK和JNK)的磷酸化水平升高,从而导致细胞凋亡。我们的研究表明,PS-MPs可激活抗氧化系统。抗氧化系统失衡调节半胱天冬酶家族,PTEN/PI3K/AKT通路引发凋亡和自噬,进而导致鸡的肺组织损伤。这些结果对PS-MPs的毒理学研究和生态系统保护具有重要意义。

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