Ethanol-Induced Alteration in Membrane Phospholipid Composition: Possible Relationship to Development of Cellular Tolerance to Ethanol

Abstract

There is now considerable evidence that unicellular organisms adapt to environmental or pharmacological agents which alter membrane fluidity by incorporating different fatty acids into the phospholipids of the cellular membranes. Two examples should suffice to illustrate the principle. Sinensky (1971) has demonstrated that E. Coli respond to increased environmental temperature by incorporating an increased proportion of saturated fatty acids into their phospholipids. Since increased temperature tends to made membranes more fluid, and the result of increasing the saturated fat content of the membrane should make it intrinsically less fluid, this can probably be regarded as an adaptive mechanism. An example of a similar mechanism in response to pharmacological manipulation is shown by the experiments of Nandini-Kishore, Kitajima and Thompson (1977) in which they demonstrated that Tetrahymena responded to the presence of a general anaesthetic, methoxyflurane, in its environment by increasing the proportion of saturated fatty acids in phospholipids. General anaesthetics are thought to act by expanding and fluidising the membrane (see Seeman, 1972) so that this response of Tetrahymena may be exactly analogous to adaptation to high environmental temperature. Ethanol, in concentrations which cause intoxicaction, has also been shown to fluidise membranes (Chin and Goldstein, 1977a) raising the possibility that tolerance to ethanol may, at least partly, be explained by an adaptation in the lipids of cell membranes.