Abstract
Chronic alcohol consumption has been identified as a significant risk factor for cancer in humans. The aim of the study was to analyze the influence of low concentrations of ethanol on gastric adenocarcinoma cell viability, apoptosis, and changes in the expression of alcohol dehydrogenase with ethanol treatment. Gastric adenocarcinoma cell lines (MGC803, MGC823 and SGC7901) were treated with different concentrations of ethanol (0.03125%, 0.0625%, 0.125%, 0.25%, 0.5%, 1%, 2%, and 4%). An MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and flow cytometry were used to analyze the effect of ethanol treatment on cell viability and apoptosis. Western blotting was used to analyze the expression of alcohol dehydrogenase in gastric carcinoma cells. Ethanol treatment inhibited cell proliferation in gastric adenocarcinoma cell lines in a significant dose-dependent manner. Ethanol was also able to induce the apoptosis of gastric adenocarcinoma cells in a dose-dependent manner. Alcohol dehydrogenase activity of gastric adenocarcinoma cells increased with the increase in the concentration of ethanol. Ethanol inhibited cell viability and growth of gastric adenocarcinoma cell lines. Low concentrations of ethanol also induced apoptosis and increased the expression of alcohol dehydrogenase of the gastric adenocarcinoma cell lines.
Highlights
Alcohol is the oldest and most widely used drug in the world
The proliferation all of the three gastric adenocarcinoma cell lines was inhibited by ethanol in a significant, dose-dependent manner
Apoptosis induced by ethanol in MGC803, BGC-823 and SGC7901 cells increased in a dose-dependent manner with the increase in the ethanol concentration (Table 1, Fig. 2)
Summary
Alcohol is the oldest and most widely used drug in the world. There are possible health benefits of consuming low levels of alcohol, while effects can be severely detrimental in cases of chronic alcohol abuse. Heavy drinking over a long period of time can lead to alcoholic liver disease. Chronic alcohol consumption has been identified as a significant risk factor for cancer in humans. Alcohol consumption increased the risk of gastric cancer in subjects with gastric atrophy (OR=2.4, p=0.03) (Yamaji et al, 2009) the exact mechanism of ethanol-associated carcinogenesis remains unknown (Jelski and Szmitkowski, 2008). Alcohol is generally metabolized via several different pathways. The breakdown of alcohol by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) is a hallmark of the most com-
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