Abstract
Erythrocyte membranes from healthy controls and alcoholic patients, examined within 24 h of abstinence, were studied for basal membrane fluidity and membrane sensitivity to ethanol by fluorescence polarization of the apolar probe 1,6-diphenyl-l, 3,5-hexatriene (DPH) and its cationic derivative l,4(tri-methylammonium phenyl)-6-phenyl-l,3,5-hexatriene (TMA-DPH). The membrane partition (Kp) of ethanol and phenobarbital, and the concentrations of membrane-bound sialic acid and galactose, were also determined. The apolar hydrocarbon region of the membrane (DPH) was less fluid, in the alcoholics than in the controls (p<p0.005). In the patients this membrane layer, as well as the polar lipid head group region (TMA-DPH), showed reduced fluidizing effect of ethanol (p<0.01). This resistance or tolerance to ethanol correlated with a markedly impaired (-59%, p<0.025) partition of ethanol into the membrane. The low Kp of ethanol in turn was partly related to reduced concentrations of polar carbohydrates such as sialic acid and galactose (p<0.01) at the membrane surface. The Kp of phenobarbital was reduced in the patients (-59%, p<0.005) but, apparently unrelated to the carbohydrate changes. These results indicate that in man, chronic alcohol abuse is associated with complex changes of membrane properties at different membrane levels e.g. at the charged surface, in the polar lipid head group region and in the hydrocarbon core. A partial basis for biophysical membrane tolerance to ethanol is suggested, implying that apart from phospholipid alterations, structural changes in membrane-bound glycoconjugates participate in this adaptive process.