Toxicology in vitro : an international journal published in association with BIBRAMar 19, 2011

High protective molecule levels do not prevent alcohol-related cell death in liver cells with increased alcohol-processing enzymes

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 2, 2026

Abstract

Chronic exposure to 100 mM ethanol for 72 hours resulted in a 47% decrease in cell viability in VL-17A cells.

VL-17A cells showed signs of apoptosis and oxidative stress compared to untreated HepG2 cells.
Chronic ethanol exposure primarily caused apoptotic cell death in VL-17A cells.
VL-17A cells exhibited a 1.1- to 2.5-fold increase in levels of alcohol dehydrogenase and CYP2E1 after ethanol treatment.
The antioxidant GSH was upregulated by 3-fold in VL-17A cells exposed to ethanol, indicating a potential metabolic adaptation.
Despite the increased GSH levels, it may not be sufficient to protect VL-17A cells from oxidative stress and apoptosis.

Simplified

Chronic consumption of alcohol leads to liver injury. Ethanol-inducible Cytochrome P450 2E1 (CYP2E1) plays a critical role in alcohol mediated oxidative stress due to its ability to metabolize ethanol. In the present study, using the recombinant human hepatoma cell line VL-17A that over-expresses the alcohol metabolizing enzymes-alcohol dehydrogenase (ADH) and CYP2E1; and control HepG2 cells, the mechanism and mode of cell death due to chronic ethanol exposure were studied. Untreated VL-17A cells exhibited apoptosis and oxidative stress when compared with untreated HepG2 cells. Chronic alcohol exposure, i.e., 100 mM ethanol treatment for 72 h caused a significant decrease in viability (47%) in VL-17A cells but not in HepG2 cells. Chronic ethanol mediated cell death in VL-17A cells was predominantly apoptotic, with increased oxidative stress as the underlying mechanism. Chronic ethanol exposure of VL-17A cells resulted in 1.1- to 2.5-fold increased levels of ADH and CYP2E1. Interestingly, the level of the antioxidant GSH was found to be 3-fold upregulated in VL-17A cells treated with ethanol, which may be a metabolic adaptation to the persistent and overwhelming oxidative stress. In conclusion, the increased GSH level may not be sufficient enough to protect VL-17A cells from chronic alcohol mediated oxidative stress and resultant apoptosis.

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High protective molecule levels do not prevent alcohol-related cell death in liver cells with increased alcohol-processing enzymes

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