Apoptosis of lung cells regulated by mitochondrial signal pathway in crotonaldehyde-induced lung injury.

Abstract

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.