Apoptosis of lung cells regulated by mitochondrial signal pathway in crotonaldehyde-induced lung injury.
apoptosis
crotonaldehyde
lung
mitochondrial pathway
toxicity
Journal
Environmental toxicology
ISSN: 1522-7278
Titre abrégé: Environ Toxicol
Pays: United States
ID NLM: 100885357
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
21
06
2019
revised:
25
05
2020
accepted:
06
06
2020
pubmed:
9
7
2020
medline:
21
10
2020
entrez:
9
7
2020
Statut:
ppublish
Résumé
Crotonaldehyde, a highly toxic α, β-unsaturated aldehyde, is a ubiquitous hazardous pollutant. Because of its extreme toxicity and ubiquity in all types of smoke, most current research focuses on the lung toxicity of such air pollutants. However, the specific mechanism of pulmonary toxicity caused by crotonaldehyde remains unclear, especially after long-term exposure to crotonaldehyde at low dose. Therefore, the aim of the present study is to determine whether crotonaldehyde-induced oxidative damage and inflammation promote apoptosis in rats via the mitochondrial pathway using histopathology, immunohistochemistry, biochemistry analysis and Western blot analysis. The results show that crotonaldehyde elicited oxidative damage and inflammation in rats in a concentration-dependent manner. Crotonaldehyde-induced lung injury which was confirmed by H&E, Masson's trichrome staining and TUNEL. And crotonaldehyde-induced lung cell apoptosis showed a concentration-response relationship. Immunohistochemistry and Western blot results showed that apoptotic mitochondrial signaling pathway is abnormally activated in crotonaldehyde-induced lung injury. Collectively, this study demonstrates that exposure of rats to crotonaldehyde induces lung injury by inducing apoptosis, which is related to oxidative damage and inflammation through mitochondrial pathway.
Substances chimiques
Aldehydes
0
Environmental Pollutants
0
2-butenal
9G72074TUW
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1260-1273Subventions
Organisme : National Natural Science Foundation of China
ID : 81602893
Organisme : Natural Science Foundation of Shandong Province
ID : ZR2015YL049
Organisme : Natural Science Foundation of Shandong Province
ID : ZR2016YL016
Informations de copyright
© 2020 Wiley Periodicals LLC.
Références
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