Chronic Ethanol Consumption Affects Glutathione Status in Rat Liver , ,

Abstract

There is no consensus yet on the role of oxidative stress in the nutritional outcome of chronic ethanol feeding and the status of cellular antioxidative defense systems against ethanol toxicity. In this study, chronic alcohol consumption in humans was reproduced in Sprague-Dawley rats to investigate the effect of ethanol ingestion on the regulation of oxidative stress in liver with a special focus on glutathione. Adult male rats were given 36% of total energy as alcohol in the Lieber-DeCarli liquid diet for 6 wk. The control group was pair-fed the diet containing isocaloric dextrin-maltose instead of ethanol. Chronic ethanol ingestion enhanced expression of cytochrome P450 II E1 in the liver, but did not significantly alter either the level of hepatic thiobarbituric acid reactive substances or the carbonyl group content of proteins. The hepatic concentrations of total and reduced glutathione and the activities of catalase, glutathione reductase and glutathione S-transferase were significantly higher in the ethanol group than in the control group. The activities of glutathione peroxidase and glucose-6-phosphate dehydrogenase were significantly lower in the ethanol group than in controls. Chronic ethanol consumption by well-nourished rats for 6 wk increased enzyme activities related to the recycling and utilization of glutathione in the liver. Such an enhancement in the activities of the hepatic antioxidative defense system may be one of the protective mechanisms of the body against oxidative tissue damage caused by ethanol-induced free radicals.

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

“…Chronic ethanol ingestion accounts for the formation of ROS and can induce a decrease of antioxidant defense. 29,30 The liver is the primary organ responsible for the oxidation of ingested ethanol. However, kidney may contribute to ethanol metabolism.…”

Increased 11β-hydroxysteroid dehydrogenase type-1 and hexose-6-phosphate dehydrogenase in liver and adipose tissue of rat offspring exposed to alcohol in utero

“…The activities of these enzymes tend to respond to similar physiological stimuli, being enhanced by oxidative stress, oxoglucocorticoids (20,55), and estrogens (28,52) but attenuated by DHEA (3,38). However, H6PD is less affected by steroids and NADPH (43) and more affected by some hepatotoxins (65) than G6PDH, while G6PDH may be inhibited by oxidants and alcohol (42,67).…”

Progression of Lipid Peroxidation Measured as Thiobarbituric Acid Reactive Substances, Damage to DNA and Histopathological Changes in the Liver of Rats Subjected to a Methionine–Choline‐Deficient Diet

“…Hepatic tissue fragments embedded in paraffin were cut into 4 lm thick sections stained with Harris haematoxylin and eosin for the semi-quantitative evaluation of hepatic steatosis classified into crosses according to the method of Oh et al [20], with some modifications. The degree of steatosis was associated with morphological location (zones 1, 2, and 3): 0 (0%); 1-25% (1: scarcely present in zone 3); 25-50% (2: zone 3); 50-75% (3: zones 2 and 3) and 75-100% (4: zones 1, 2 and 3).…”