Cytotoxicity of short-chain alcohols

Ethanol and other short-chain alcohols elicit a number of cellular response s that are potentially cytotoxic and, to some extent, independent of cell t ype. Aberrations in phospholipid and fatty acid metabolism, changes in the cellular redox state, disruptions of the energy state, and increased produc tion of reactive oxygen metabolites have been implicated in cellular damage resulting from acute or chronic exposure to short-chain alcohols. Resultin g disruptions of intracellular signaling cascades through interference with the synthesis of phosphatidic acid, decreases in phosphorylation potential and lipid peroxidation are mechanisms by which solvent alcohols can affect the rate of cell proliferation and, consequently, cell number. Nonoxidativ e metabolism of short-chain alcohols, including phospholipase D-mediated sy nthesis of alcohol phospholipids, and the synthesis of fatty acid alcohol e sters are additional mechanisms by which alcohols can affect membrane struc ture and compromise cell function.