title: Effects of chronic alcohol feeding and murine AIDS virus infection on liver antioxidant defense systems in mice.
abstract: Whether ethanol (ETOH) abuse could contribute to the development of acquired immunodeficiency syndrome (AIDS) among human immunodeficiency virus (HIV)-positive drug abusers is a critical question for which little experimental information is available. This study was designed to determine if chronic ETOH feeding and murine AIDS virus infection cooperatively affected liver antioxidant defense systems in C57B1/6 female mice. Mice were divided into two groups and fed the Lieber-DeCarli liquid ETOH diet containing ETOH at a concentration to provide 31% of total caloric intake or an isocaloric liquid control (control) diet in which dextrin-maltose replaced ETOH. One week after the initiation of ETOH feeding, half of the mice in each diet group (8 mice) were injected intraperitoneally with murine retrovirus (MAIDS) stock. After 3 and 5 weeks of ETOH feeding, half of the mice in each of the four treatment groups (4 mice) were killed, and livers were excised for biochemical analysis. Liver reduced glutathione (GSH) levels and activities of glutathione peroxidase (GP), glutathione reductase (GR), glutathione transferase (GT), catalase and superoxide dismutase (SOD), and serum ETOH concentrations were determined. The results demonstrated that serum ETOH concentrations were significantly elevated in ETOH-MAIDS group when compared with the ETOH group. Moreover, chronic ETOH feeding and MAIDS infection independently depressed liver antioxidant defense capability, and together led to an additive inhibition of GSH and SOD activities. In addition, MAIDS infection inhibited an ETOH-induced increase in catalase and GT activities. These results suggest that alcohol abuse could contribute to the development of AIDS by inhibiting the protective capability of an infected individual against oxidative stress.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Nutrition and Food Science, University of Kentucky, Lexington.
authors.forename: L H
authors.initials: LH
authors.lastname: Chen
authors.forename: C Y
authors.initials: CY
authors.lastname: Huang
authors.forename: Y
authors.initials: Y
authors.lastname: Osio
authors.forename: E A
authors.initials: EA
authors.lastname: Fitzpatrick
authors.forename: D A
authors.initials: DA
authors.lastname: Cohen
mesh_terms: D000818:Animals; D000431:Ethanol / Q000493:pharmacokinetics / Q000633:toxicity; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism*; D005980:Glutathione Reductase / Q000378:metabolism*; D005982:Glutathione Transferase / Q000378:metabolism*; D008658:Inactivation, Metabolic / Q000502:physiology; D008099:Liver / Q000187:drug effects / Q000503:physiopathology; D008108:Liver Diseases, Alcoholic / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016183:Murine Acquired Immunodeficiency Syndrome / Q000503:physiopathology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species; D000431:Ethanol; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase