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Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption
Author(s) -
Tian Junqiang,
Brown Lou Ann S.,
Jones Dean P.,
Levin Marc S.,
Wang Lihua,
Rubin Deborah C.,
Ziegler Thomas R.
Publication year - 2009
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607109336600
Subject(s) - glutathione , chemistry , oxidative stress , ileum , glutathione disulfide , liquid diet , ingestion , medicine , endocrinology , jejunum , malondialdehyde , lipid peroxidation , biochemistry , redox , ethanol , intestinal mucosa , organic chemistry , enzyme
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.