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

Zhenjing Li,Jingkai Zhang,Cheng Luo,Yibin Xue,Xiaohong Zhang,Meiling Li

doi:10.1155/2018/6864574

Zhenjing Li, Jingkai Zhang + Show 4 more

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https://doi.org/10.1155/2018/6864574

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Abstract

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.

Highlights

Acetaldehyde in the human body is primarily oxidized and metabolized by alcohol dehydrogenase in the liver
Influence of Acetaldehyde and L-Cys on Cell Viabilities of A549 Cells. e cell viability of A549 cells decreased within the range of 0 μmol/L to 900 μmol/L of acetaldehyde (Figure 1(a)) in a dose-dependent manner, which indicates that acetaldehyde can inhibit cell proliferation
L-Cys Influences GSH-Px Activity in A549 Cell Damaged by Acetaldehyde

Summary

Introduction

Acetaldehyde in the human body is primarily oxidized and metabolized by alcohol dehydrogenase in the liver. Its low boiling point (20.2°C) causes acetaldehyde to evaporate . E perception limit of acetaldehyde in air ranges from 0.07 mg/L to 0.25 mg/L, which is within the normal range of concentrations for fruity odor [1]. Acetaldehyde has been shown to act on the liver by depressing mitochondrial function, decreasing fatty acid oxidation, enhancing glycogenolysis, and decreasing gluconeogenesis from glycerol during alcohol consumption [3]. Acetaldehyde reacts with DNA to form a variety of adducts that may cause polymerase errors and mutations in critical genes, frequently activating proto-oncogenes while inactivating tumor suppressor genes to result in tumorigenesis or carcinogenesis [4,5,6]. Acetaldehyde is considered as a major cause of alcoholism and alcohol addiction [7, 8]. erefore, the effective elimination of acetaldehyde is important in preventing cellular toxicity and in the efficient removal of alcohol [9]

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