Chronic and acute ethanol treatment modifies fluidity and composition in plasma membranes of a human hepaic cell line (WRL-68)

Abstract

The aim of this study was to compare the effects of chronic (0.1 mol/L ethanol exposure during 30 days) and acute (0.5 mol/L ethanol exposure during 24 h) ethanol treatment on the physical properties and the lipid composition of plasma membranes of the WRL-68 cells (fetal human hepatic cell line). Using fluorescence polarization we found that ethanol treatment reduced membrane anisotropy due to disorganization of acyl chains in plasma membranes and consequently increased fluidity, as measured with the diphenylhexatriene probe. Addition of ethanol in vitro reduced anisotropy in control plasma membranes, whereas chronically ethanol-treated plasma membranes were relatively tolerant to the in vitro addition of ethanol. Acutely ethanol-treated plasma membranes exhibited a smaller anisotropy parameter value than control plasma membranes. We found a decrease in total phospholipid content in acute ethanol WRL-68 plasma membranes. Cholesterol content was increased in both ethanol treatments, and we also found a significant decrease in phosphatidylinositol and phosphatidylcholine and an increase in phosphatidylethanolamine content in ethanol-treated plasma membranes. Our data showed that ethanol treatment decreased the anisotropy parameter consistently with increased fluidity, while increasing the cholesterol/phospholipid ratio of plasma membranes of WRL-68 cells, but only chronically ethanol-treated plasma membranes exhibited tolerance to the in vitro addition of ethanol. It is important to note that some changes that were interpreted as a result of chronic ethanol treatment were also present in short-period ethanol treatments.

Effects of Different Quantities of Fat on Serum and Liver Lipids, Phospholipid Class Distribution and Fatty Acid Composition in Alcohol-Treated Rats

“…In our study the CH/PL liver molar ratio was significantly higher in the liver of alcohol-treated rats with a different amount of dietary fat, because total phospholipid content de creased with no difference in cholesterol content in the liver according to alcohol intake. In contrast to previous studies, Gutierez-Ruin et al (35) showed that alcohol intake increased fluidity with an increase in the CH/PL liver molar ratio of plasma membranes. They found a decrease in phospholid content after acute alcohol intake and increased cholesterol content in acute and chronic treatments in the liver plasma membrane.…”

Neuroprotection by taurine in ethanol-induced apoptosis in the developing cerebellum

“…The effects of alcohol on biological membranes depend on the duration of its administration. Acute ethanol administration increases the membrane fluidity [60-62], whereas chronic alcohol intake decreases the fluidity of membranes [60,63,64], which become more tolerant to the disordering effect of ethanol [60,63]. Acute ethanol exposure also decreases Na + /K + -ATPase activity in the cerebral cortex and brain stem [65] and kidneys of adult rats [66].…”

Role for Membrane Fluidity in Ethanol-Induced Oxidative Stress of Primary Rat Hepatocytes

“…It can result from ethanol metabolism in hepatocytes that triggers reactive oxygen species (ROS) production during both acute and chronic alcoholism (Sergent et al, 1995;Bailey and Cunningham, 1998). At the very early stage of the disease, changes in membrane fluidity could also play a role, because an increase in plasma membrane fluidity has been described after acute ethanol intoxication of WRL-68 hepatic cell lines (Gutierrez-Ruiz et al, 1995) or of primary rat hepatocytes (Benedetti et al, 1994). What is particularly interesting is that liver is the only organ to maintain this increase in membrane fluidity during chronic intoxication (Yamada and Lieber, 1984;Polokoff et al, 1985), even though chronic ethanol exposure of animals or liver cells would make membranes more resistant to the disordering effects of ethanol in vitro (Polokoff et al, 1985;GutierrezRuiz et al, 1995).…”