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Ethanol preconditioning prevents ischemia‐reperfusion‐induced mitochondrial dysfunction in intestinal mucosa by an adenosine‐dependent mechanism in rats
Author(s) -
Kalogeris Theodore J.,
Wang Qun,
Gaskin F. Spencer,
Wang Meifang,
Korthuis Ronald J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.730.9
Subject(s) - enterocyte , adenosine , adenosine receptor , mitochondrion , ischemia , agonist , pharmacology , chemistry , antagonist , medicine , endocrinology , receptor , biology , biochemistry , small intestine
Ethanol preconditioning (EPC) protects tissues from ischemia‐reperfusion (IR)‐induced injury by an unknown mechanism. Whereas ischemic preconditioning prevents IR‐induced mitochondrial dysfunction, it is unknown whether EPC has a similar protective effect. We tested this question in rats subjected to intestinal IR (20 min ischemia, 60 min reperfusion), 24 h after either control or ethanol (0.63 ml/kg) gavage, assaying mucosal mitochondrial respiration (MR), enterocyte mitochondrial membrane potential (MMP), and levels of mitochondrial cytochrome c. Compared with sham‐treated rats, IR decreased enterocyte mitochondrial respiratory function, membrane potential and cytochrome c content by 77%, 67%, and 61%, respectively. These effects were completely reversed in EPC rats. The protective effects of ethanol on MR and MMP were prevented in rats administered DMPX (adenosine A2 receptor antagonist), 10 min prior to EPC treatment; ethanol's protective effect on MMP was reproduced by administration of CPCA, an adenosine A2 receptor agonist. These results support the hypothesis that EPC prevents intestinal mucosal mitochondrial dysfunction through an adenosine‐dependent mechanism. Supported by AA14945 and DK43785.