Autophagy in exposure to environmental chemicals.
Autophagosome
Nanoparticles
Particulate matter
Pesticides
Tobacco smoke
Journal
Toxicology letters
ISSN: 1879-3169
Titre abrégé: Toxicol Lett
Pays: Netherlands
ID NLM: 7709027
Informations de publication
Date de publication:
01 May 2019
01 May 2019
Historique:
received:
12
07
2018
revised:
06
11
2018
accepted:
18
01
2019
pubmed:
22
1
2019
medline:
23
2
2019
entrez:
22
1
2019
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 30664929
pii: S0378-4274(19)30009-8
doi: 10.1016/j.toxlet.2019.01.007
pii:
doi:
Substances chimiques
Environmental Pollutants
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-9Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.