Drug Discov Ther. 2007;1(2):130-135.

The effects of antidepressant drug on ethanol-induced cell death.

Johnson S, Williams AN, Johnson C, Ou XM


Alcoholism is a serious health problem. Alcohol-dependent subjects have many health-related problems, such as severe cognitive impairments, alcoholic liver disease and coronary heart disease, resulting from ethanol-induced cell injury or cell death. Understanding the mechanisms underlying the cell death may provide clues for novel treatment strategies to prevent alcohol-induced cell damage. Prolonged ethanol consumption causes apoptotic activity in a host of cell types – more obviously affecting the liver, heart and surprisingly affecting the brain. This study uses four cell lines: neuronal cell line (SH-SY5Y), glia cell line (U-118 MG), liver cell line (E47) and heart cell line (the rat H9c2), and addresses that alcohol does, in fact, cause cell death in these four cell types, whether ethanol induced cell death is through apoptotic pathway, and whether an monoamine oxidase (MAO) inhibitor (e.g. deprenyl) protects cells from the effects of alcohol. We have found that ethanol exposure lowers cell proliferation in all cell types, but affects brain cell lines (neuron and glioma) the most, while ethanol and deprenyl exposure in unison increases cell viability largely in brain cells, and then in liver cells. Our results suggest that MAO mediated apoptosis may contribute to ethanolinduced cell death. Individuals suffering from alcoholism or alcohol abuse may be treated with deprenyl to alleviate the apoptotic activity resulting from alcohol consumption and protect the body’s cells from alcohol-induced death. In summary, this study demonstrates the effects of deprenyl as an anti-apoptotic agent against the detrimental effects of alcohol.

KEYWORDS: Alcohol, neuroblastoma, glioma, cell culture, cell viability

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