Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine

Acetaldehyde is a harmful metabolite of smoking and drinking. This study was initially intended to facilitate the understanding of the possible injury mechanism of A549 cells damaged by acetaldehyde and the possible protective mechanism of L-cysteine (L-Cys) by analyzing the oxidative damage indicat...

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Main Authors: Zhenjing Li, Xiaohong Zhang, Yibin Xue, Jingkai Zhang, Meiling Li, Cheng Luo
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Journal of Chemistry
Online Access:http://dx.doi.org/10.1155/2018/6864574
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author Zhenjing Li
Xiaohong Zhang
Yibin Xue
Jingkai Zhang
Meiling Li
Cheng Luo
author_facet Zhenjing Li
Xiaohong Zhang
Yibin Xue
Jingkai Zhang
Meiling Li
Cheng Luo
author_sort Zhenjing Li
collection DOAJ
description Acetaldehyde is a harmful metabolite of smoking and drinking. This study was initially intended to facilitate the understanding of the possible injury mechanism of A549 cells damaged by acetaldehyde and the possible protective mechanism of L-cysteine (L-Cys) by analyzing the oxidative damage indicators, as well as the changes in cell morphology and gene expression. Results from the dithiodimorpholine nitrobenzoic acid colorimetric determination for glutathione peroxidase (GSH-Px) activity in L-Cys groups were significantly higher (P<0.01) than those in the acetaldehyde group in a dose-dependent manner. The expression of cytochrome c oxidase subunit II (COII) mRNA was significantly reduced compared with the control group (P<0.01) and was noticeably restored in the L-Cys groups. Scanning electronic microscopy observation, DAPI staining, and flow cytometry also indicated that L-Cys could effectively attenuate the oxidative damage to A549 cells caused by acetaldehyde and reduces the rate of apoptosis. In conclusion, the protective effects of L-Cys on A549 cells against oxidative damage by acetaldehyde were dose-dependent within the range of 10 μmol/L to 160 μmol/L. Acetaldehyde damaged the mitochondria and resulted in the apoptosis of A549 cells by reactive oxygen species (ROS), e.g., free radicals, but L-Cys reversed the release of cytochrome c from the mitochondria, reduced the rate of apoptosis, and protected cells from ROS and oxidative stress.
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spelling doaj-art-b027332c23d741b69d528e13a55846182025-08-20T02:19:18ZengWileyJournal of Chemistry2090-90632090-90712018-01-01201810.1155/2018/68645746864574Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-CysteineZhenjing Li0Xiaohong Zhang1Yibin Xue2Jingkai Zhang3Meiling Li4Cheng Luo5State Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, ChinaState Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, ChinaState Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, ChinaState Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, ChinaState Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, ChinaState Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, ChinaAcetaldehyde is a harmful metabolite of smoking and drinking. This study was initially intended to facilitate the understanding of the possible injury mechanism of A549 cells damaged by acetaldehyde and the possible protective mechanism of L-cysteine (L-Cys) by analyzing the oxidative damage indicators, as well as the changes in cell morphology and gene expression. Results from the dithiodimorpholine nitrobenzoic acid colorimetric determination for glutathione peroxidase (GSH-Px) activity in L-Cys groups were significantly higher (P<0.01) than those in the acetaldehyde group in a dose-dependent manner. The expression of cytochrome c oxidase subunit II (COII) mRNA was significantly reduced compared with the control group (P<0.01) and was noticeably restored in the L-Cys groups. Scanning electronic microscopy observation, DAPI staining, and flow cytometry also indicated that L-Cys could effectively attenuate the oxidative damage to A549 cells caused by acetaldehyde and reduces the rate of apoptosis. In conclusion, the protective effects of L-Cys on A549 cells against oxidative damage by acetaldehyde were dose-dependent within the range of 10 μmol/L to 160 μmol/L. Acetaldehyde damaged the mitochondria and resulted in the apoptosis of A549 cells by reactive oxygen species (ROS), e.g., free radicals, but L-Cys reversed the release of cytochrome c from the mitochondria, reduced the rate of apoptosis, and protected cells from ROS and oxidative stress.http://dx.doi.org/10.1155/2018/6864574
spellingShingle Zhenjing Li
Xiaohong Zhang
Yibin Xue
Jingkai Zhang
Meiling Li
Cheng Luo
Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
Journal of Chemistry
title Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
title_full Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
title_fullStr Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
title_full_unstemmed Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
title_short Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
title_sort cellular and molecular evidence of acetaldehyde elimination and intracellular environment antioxidation by l cysteine
url http://dx.doi.org/10.1155/2018/6864574
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