ETHANOL-INDUCED OXIDATIVE STRESS AND NUTRITIONAL-STATUS

The ability of dietary ethanol, administered over a 10-day period, to elevate production rates of reactive oxygen species and to alter glutathione levels has been determined in both liver and cerebellum, a brain region known to be susceptible to ethanol-induced damage. Two groups of ethanol-consuming rats were used. One set of treated animals that received an all-liquid ethanol-containing diet experienced weight gain, and this gain was matched in a pair-fed control group. The other ethanol-treated group that had free access only to solid chow and water containing ethanol lost weight during the' exposure period. The corresponding control group that received unlimited water and chow was allowed to gain weight normally. In animals that lost weight as a consequence of ethanol in the drinking water, evidence of oxidative stress was enhanced relative to that in animals receiving ethanol by way of the liquid diet. This latter set gained weight, despite higher blood ethanol levels than the group that lost weight. An excess prooxidant condition prevailed in the liver and cerebellum of the ethanol-dosed malnourished group. In the case of liver, this difference may relate to a greater lability of iron-containing proteins in the rats that experienced weight loss, leading to the appearance of low molecular weight iron in the cytosol.