J Korean Med Sci.  1997 Aug;12(4):316-321. 10.3346/jkms.1997.12.4.316.

Glutathione recycling is attenuated by acute ethanol feeding in rat liver

• Oh SI
• Kim CI
• Chun HJ
• Lee MS
• Park SC

• KMID: 1081053
• DOI: http://doi.org/10.3346/jkms.1997.12.4.316

Abstract

The mechanism for ethanol-induced oxidative stress has been disputed because of the controversies on modulation of radical generating and scavenging activities by ethanol. In the present work, we attempted to clarify the acute effect of ethanol on the radical generating system as well as the radical scavenging system. For that purpose, chow-fed rats were given ethanol (5 g/kg) or isocaloric glucose solution by intragastric intubation and placed at 32 degrees C for 6 hr. Acute ethanol administration enhanced the expression of cytochrome P450 II E1(CYP II E1) in the liver and attenuated the activities of hepatic glutathione peroxidase (GPx) and reductase (GR). It also caused a significant increase in the level of hepatic thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation. On the other hand, acute ethanol feeding had no effect on the activities of catalase, xanthine oxidase (XO), glutathione transferase (GST) and glucose-6-phosphate dehydrogenase (G6PDH). From this result, it is suggested that acute ethanol administration causes the oxidative tissue damage by CYP II E1-associated radical generation and the decreased radical scavenging function due to the reduced activities of hepatic glutathione recycling system such as GPx and GR.

MeSH Terms

Alcohol Drinking/metabolism*
Animal
Antioxidants/metabolism
Free Radical Scavengers
Glutathione/metabolism*
Lipid Peroxidation/drug effects*
Liver/metabolism
Liver/enzymology
Liver/drug effects*
Male
Oxidative Stress/physiology
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species/metabolism