ABSTRACT
The effects of ethanol (EtOH) on membrane fatty acid composition have been intensely studied and reviewed.1-4 EtOH-induced reductions in long-chain, polyunsaturated fatty acid (PUFA) levels were reported in adult brain3-9 and in adult retina.9 EtOH-induced reductions in membrane PUFA levels were also reported in adult liver10-12 and adult erythrocytes.13 In adult liver membranes, reduced levels of long-chain polyunsaturated membrane fatty acids (PUFAs) correlated with alcohol-induced liver damage14,15 and decreased levels of long-chain PUFAs were reported during necrosis and apoptosis.16-19
These EtOH-induced changes in membrane fatty acid composition may partially explain EtOH-induced changes in membrane fluidity.4,20-22 In many systems, EtOHinduced increases in membrane fluidity have been observed in membranes isolated from EtOH-intolerant animals. Meanwhile, membranes isolated from EtOH-tolerant animals resist the fluidizing effects of EtOH. These observations led to an interesting hypothesis by Hagai Rottenberg and colleagues23-25 who speculated that EtOH-induced increases in membrane fluidity are damaging while the ability to resist EtOH-induced increases in membrane fluidity in EtOH-tolerant animals is a component of EtOH-tolerance. In EtOHdependency, EtOH may be required to fluidize overly nonfluid and nonfunctional membranes into near normal levels of membrane fluidity and may be required to reestablish normal membrane functionality.
