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Journal of Parenteral and Enteral Nutrition
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Original Communications

Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption

Junqiang Tian, PhD1,2, Lou Ann S. Brown, PhD1,3,4, Dean P. Jones, PhD1,2,3, Marc S. Levin, MD5,6, Lihua Wang5, Deborah C. Rubin, MD5 and Thomas R. Ziegler, MD1,2,3

From the 1 Nutrition and Health Science Program, Graduate School of Arts and Science, Emory University, Atlanta, Georgia; the2 Department of Medicine and the3 Center for Clinical and Molecular Nutrition, Emory University School of Medicine, Atlanta, Georgia; the4 Department of Pediatrics, Emory University, Atlanta, Georgia; the 5 Department of Medicine, Washington University School of Medicine, St Louis, Missouri; and6 Specialty Care Service Line, St Louis VA Medical Center, St Louis, Missouri.

Address correspondence to: Thomas R. Ziegler, MD, Atlanta Clinical and Translational Science Institute, Room GG-23, Emory University Hospital, 1364 Clifton Road, Atlanta, GA 30322; e-mail: tzieg01{at}emory.edu.

Background: Alcohol consumption is associated with oxidative stress in multiple tissues in vivo, yet the effect of chronic alcohol intake on intestinal redox state has received little attention. In this study, we investigated the redox status of 2 major intracellular redox regulating couples: glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) in a rat model of chronic alcohol ingestion. Methods: Sprague-Dawley rats were fed the liquid Lieber-DeCarli diet consisting of 36% ethanol of total calories for 6 weeks. Control rats were pair-fed with an isocaloric, ethanol-free liquid diet. Defined mucosal samples from the jejunum, ileum, and colon were obtained and analyzed by high-performance liquid chromatography (HPLC) for GSH and Cys pool redox status. Mucosal free malondialdehyde (MDA) was measured as an indicator of lipid peroxidation. Results: In the ethanol-fed rats, Cys and mixed disulfide (GSH-Cys) were significantly decreased in all 3 segments of intestinal mucosa. Free MDA was increased in jejunal but not in ileal or colonic mucosa. Chronic ethanol ingestion significantly increased mucosal GSH concentration in association with a more reducing GSH/GSSG redox potential in the jejunum, but these indices were unchanged in the ileum. In the colon, chronic ethanol ingestion increased oxidant stress as suggested by decreased GSH and oxidized GSH/GSSG redox potential. Conclusions: Chronic alcohol intake differentially alters the mucosal redox status in proximal to distal intestinal segments in rats. Such changes may reflect different adaptability of these intestinal segments to the oxidative stress challenge induced by chronic ethanol ingestion.

Key Words: alcohol • intestine • redox • GSH • Cys

This version was published on November 1, 2009

Journal of Parenteral and Enteral Nutrition, Vol. 33, No. 6, 662-668 (2009)
DOI: 10.1177/0148607109336600


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