Enhanced sensitivity of pituitary beta-endorphin to ethanol in subjects at high risk of alcoholism.
ABSTRACT Previous studies have demonstrated that a moderate dose of ethanol induced a significant increase in the plasma beta-endorphin content of subjects from families with a history of alcoholism (high risk (HR)), but not subjects from families without a history of alcoholism (low risk (LR)). The objective of this study was to examine the response of the pituitary beta-endorphin and adrenal cortisol systems to various concentrations of ethanol in male and female subjects at high and low risk of the future development of alcoholism.
All subjects participated in four experimental sessions. In each session the subjects were given a drink containing one of the following doses of ethanol: 0, 0.25, 0.50, and 0.75 g of ethanol per kilogram of body weight (for a 60- to 70-kg individual). Blood samples were taken at 0 minutes and at 15, 45, 120, and 180 minutes after the drink for estimation of the blood alcohol, plasma beta-endorphin, and plasma cortisol levels.
The concentration of alcohol in the blood at various intervals after the drink was similar among the subjects, regardless of the risk group. Ethanol increased the plasma level of beta-endorphin-related peptides of the HR but not of the LR subjects in a dose-dependent manner. All subjects showed a small decrease in plasma cortisol level with time, but ethanol ingestion did not significantly alter the plasma cortisol levels.
This study indicates that the pituitary beta-endorphin system, but not the adrenal cortisol system, of the HR subjects shows an enhanced sensitivity to ethanol, which may be an important factor in controlling ethanol consumption.
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ABSTRACT: The effect of ethanol consumption was investigated in 262 Wistar rats by using several methods of its administration on the development of adjuvant arthritis (AA). The results showed that the self-consumption of 10% alco-hol to some degree promotes the development of inflammatory and auto-immune process in rats preferring ethanol, and this effect was more expres-sed in male rats at the end of experiment. In experiments with intragastric injections of ethanol, the effect on the development of AA depended on the duration of alcoholization. Alcoholization during one week before the reproduction of AA and the subsequent daily injections of it during the whole experiment intensified the autoimmune process, but the same injec-tions of alcohol showed no such effect on the established AA. Direct daily microinjections (10 µl) of 45% ethanol into the lateral brain ventricles intensified the inflammatory process in joints, development of polyarthritis and impaired the blood indices. The use of ethanol solutions with acetyl-salicylic acid (ASA) decreased the antiinflammatory action of ASA. Repe-ated 10% ethanol intragastric injections in combination with ASA led to an increase in plasma beta-endorphin (β-E) level in comparison with control group. Higher ethanol doses decreased plasma β-E and the effect was dose dependent. Thus, chronic ethanol consumption led to a certain impairment of AA and its action depended on the dose and scheme of alcohol administration. Alterations were greater in the groups that received alcohol infusions intra-cerebroventricularly.
- Alcoholism-clinical and Experimental Research - ALCOHOL CLIN EXP RES. 01/2006;