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环境化学物质暴露中的自噬作用。

Autophagy in exposure to environmental chemicals.

机构信息

Faculty of Health Science, School of Pharmacy/Toxicology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.

Faculty of Health Science, School of Pharmacy/Toxicology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.

出版信息

Toxicol Lett. 2019 May 1;305:1-9. doi: 10.1016/j.toxlet.2019.01.007. Epub 2019 Jan 19.

DOI:10.1016/j.toxlet.2019.01.007
PMID:30664929
Abstract

Autophagy is a catabolic pathway, which breaks down old and damaged cytoplasmic material into basic biomolecules through lysosome-mediated digestion thereby recycling cellular material. In this way, autophagy prevents the accumulation of damaged cellular components inside cells and reduces metabolic stress and toxicity. The basal level of autophagy is generally low but essential for maintaining the turnover of proteins and other molecules. The level is, however, increased in response to various stress conditions including chemical stress. This elevation in autophagy is intended to restore energy balance and improve cell survival in stress conditions. However, aberrant and/or deficient autophagy may also be involved in the aggravation of chemical-caused insults. Thus, the overall role of autophagy in chemical-induced toxicity is complex and only a limited number of environmental chemicals have been studied from this point of view. Autophagy is associated with many of the chemical-caused cytotoxic mechanisms, including mitochondrial dysfunction, DNA damage, oxidative stress, changes in the endoplasmic reticulum, impairment of lysosomal functions, and inflammation. This mini-review describes autophagy and its involvement in the responses to some common environmental exposures including airborne particulate matter, nanoparticles and tobacco smoke as well as to some common single environmental chemicals.

摘要

自噬是一种分解代谢途径,通过溶酶体介导的消化作用将衰老和受损的细胞质物质分解为基本生物分子,从而回收细胞物质。通过这种方式,自噬可以防止细胞内受损的细胞成分积累,并减少代谢应激和毒性。自噬的基础水平通常较低,但对于维持蛋白质和其他分子的周转率是必不可少的。然而,自噬水平会响应各种应激条件(包括化学应激)而增加。这种自噬的增加旨在恢复能量平衡,并在应激条件下提高细胞存活率。然而,异常和/或缺乏自噬也可能参与化学引起的损伤加重。因此,自噬在化学诱导毒性中的整体作用是复杂的,并且仅从这个角度研究了有限数量的环境化学物质。自噬与许多化学引起的细胞毒性机制有关,包括线粒体功能障碍、DNA 损伤、氧化应激、内质网变化、溶酶体功能障碍和炎症。这篇综述描述了自噬及其在对一些常见的环境暴露(包括空气颗粒物、纳米颗粒和烟草烟雾)以及一些常见的单一环境化学物质的反应中的作用。

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