Modulations of rabbit erythrocyte ATPase activities induced by in vitro and in vivo exposure to ethanol

Abstract

Alcohol intake is associated with numerous degenerative disorders, and the detrimental effects of alcohol may be due to its influence on plasma membrane and cellular transport systems. The aim of the present study was to compare in vitro and in vivo effects of ethanol on rabbit erythrocyte ATPase activities and correlate them with ethanol-induced oxidative stress. Age-matched male rabbits were given 5% ethanol in 2% sucrose solution, for 6 weeks ad libitum; control animals were given tap water. Daily intake of ethanol was 5 g/kg body weight; this experimental regimen resulted in an average serum ethanol concentration of 16.77 +/- 2.00 mM/l. After this period, blood was collected, serum ethanol concentration was determined and erythrocyte membranes were prepared according to the method of Post et al. Activities of Na(+)/K(+)- and Mg(2+)-ATPases were determined. Thiobarbituric acid-reactive substance (TBARS) assay was used to detect levels of lipid peroxidation, a major indicator of oxidative stress. In vitro ethanol inhibits both Na(+)/K(+)-ATPase and Mg(2+)-ATPase, but Na(+)/K(+)-ATPase is more sensitive to the ethanol-induced inhibition. Increasing concentration of ethanol increased TBARS production, but significant difference was attained only at 5 and 12.5 mM of ethanol. Chronic ethanol consumption induced significant increase in Na(+)/K(+)- and Mg(2+)-ATPase activity, and TBARS production. Our results suggest that increased ATPase activity induced by chronic ethanol consumption is due to oxidative, induced modification of membrane phospholipids and proteins, which are responsible for inhibition of ATPase activity. Increased production of TBARS induced by in vitro exposure to ethanol is not the only factor that influences ATPases activity. Further research is needed to elucidate this relationship.

Astaxanthin Is Able to Prevent Alcohol-Induced Dysfunction of Liver Mitochondria

“…Ethanol is also capable to change the activities of the respiratory chain complexes, and the information on this is rather contradictory. For example, in the 1990s–2000s, studies appeared on the increase in the activity of ATPase under the action of ethanol [ 55 , 56 ]. At the same time, a decrease in the activity and expression of complexes in chronic alcoholism was also shown [ 39 , 57 , 58 ].…”

Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo

“…By decreasing the activity of the Na-K-ATPase, moderate ethanol may decrease BBM glutamine co-transport by affecting the sodium gradient necessary for this co-transporter to properly function. Other studies have investigated the effect of ethanol on Na-K-ATPase activity and found that acute doses of ethanol decreased the activity of the Na-K-ATPase but chronic doses of ethanol increased its activity [33,34,35]. In all, while ethanol clearly has a wide range of effects on the Na-K-ATPase, the effect of moderate ethanol on the BLM Na-K-ATPase appears to have a role in regulating sodium-dependent nutrient assimilation by enterocytes ex vivo and in vitro.…”

The Influence of Alcohol Consumption on Intestinal Nutrient Absorption: A Comprehensive Review

“…Furthermore, following treatment with ethanol, both cellular stress responses, such as the induction of heat shock protein 70, and immune responses, such as leukocyte infiltration and histamine release, were altered in the small intestine [ 1 , 41 , 59 ]. Increases in lipid peroxidation, reduction in antioxidants, and increases in oxidative stress have also been shown to occur in response to ethanol [ 61 , 62 , 63 ]. Overall, exposure to ethanol clearly alters intestinal homeostasis, including nutrient absorption [ 1 ].…”