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Ecotoxicol Environ Saf. 2019 Jan 15;167:169-177. doi: 10.1016/j.ecoenv.2018.10.008. Epub 2018 Oct 15.

Autophagy induced by low concentrations of crotonaldehyde promotes apoptosis and inhibits necrosis in human bronchial epithelial cells.

Author information

1
Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou 450001, PR China; Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhongshan Road, Dalian 116023, PR China; University of Chinese Academy of Sciences, 19 Yuquan Road, Shijingshan District, Beijing 100049, PR China.
2
Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou 450001, PR China. Electronic address: lixiang79ben@sina.com.
3
Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, 27 Taiping Road, Beijing 100850, PR China.
4
Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou 450001, PR China. Electronic address: ztridicp@126.com.

Abstract

Crotonaldehyde is a common environmental contaminant. Autophagy, apoptosis, and necrosis, were all respectively reported to be induced by crotonaldehyde. However, the relationships between programmed cell deaths, especially between autophagy and apoptosis, have not been elucidated. In the present study, alterations of autophagy, apoptosis and necrosis were investigated in human bronchial epithelial cells (BEAS-2B) exposed to crotonaldehyde, and effects of autophagy on apoptosis and necrosis were detected. We found that a high concentration (160 μmol/L, μM) of crotonaldehyde did not induce apoptosis, while a low concentration (80 μM) of crotonaldehyde induced autophagy, apoptosis and necrosis. In 80 μM crotonaldehyde-exposed BEAS-2B cells, autophagy and apoptosis exhibited a trend of increasing prior to decreasing with the increase of time, while the time point inducing the highest level of autophagy was 2 h, and that of apoptosis was 4 h. With the pretreatment of bafilomycin A1, the apoptosis was inhibited and the necrosis was enhanced significantly in cells exposed to 80 μM crotonaldehyde. Autophagy mediated the induction of apoptosis via the intrinsic apoptotic pathway. The results indicate that autophagy mediates the initiation of apoptosis and plays a role in protecting from necrosis in low concentrations of crotonaldehyde-exposed BEAS-2B cells.

KEYWORDS:

Apoptosis; Autophagy; Crotonaldehyde; Necrosis; Programmed cell deaths

PMID:
30336407
DOI:
10.1016/j.ecoenv.2018.10.008
[Indexed for MEDLINE]

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