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Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Local Glutathione Redox Status Does Not Regulate Ileal Mucosal Growth after Massive Small Bowel Resection in Rats¹

² Nutrition and Health Science Program, Graduate School of Arts and Sciences, Emory University, Atlanta, GA 30322; ³ Department of Medicine and ⁴ Center for Clinical and Molecular Nutrition, Emory University School of Medicine, Atlanta, GA 30322; ⁵ Department of Surgery, Toho University School of Medicine, Tokyo, Japan; and ⁶ Specialty Care Service Line, St. Louis VA Medical Center, St Louis, MO 63106; and ⁷ Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110

^* To whom correspondence should be addressed. E-mail: tzieg01{at}emory.edu.

Glutathione (GSH) concentration affects cell proliferation and apoptosis in intestinal and other cell lines in vitro. However, in vivo data on gut mucosal GSH redox status and cell turnover are limited. We investigated the effect of altered GSH redox status on the ileal mucosa in a rat model of short bowel syndrome following massive small bowel resection (SBR). Rats underwent 80% mid-jejunoileal resection (RX) or small bowel transection (TX; as operative controls), with administration of either saline or D, L-buthionine-sulfoximine (BSO), a specific inhibitor of cellular GSH synthesis. Ileal mucosal redox, morphology, and indices of cell proliferation and apoptosis were determined at different days after surgery. Ileal GSH redox status was assessed by GSH and GSH disulfide (GSSG) concentrations and the redox potential of GSH/GSSG (E_h). Ileal lipid peroxidation [free malondialdehyde (MDA)] was measured as an index of lipid peroxidation. BSO markedly decreased ileal mucosal GSH, oxidized GSH/GSSG E_h, and increased MDA content without inducing morphological damage as assessed by light or electron microscopy. As expected, SBR stimulated adaptive growth of ileal villus height and total mucosal height at 7 d after surgery, but this response was unaffected by BSO treatment despite a modest increase in crypt cell apoptosis. Ileal cell proliferation (crypt cell bromodeoxyuridine incorporation) increased at 2 d after SBR but was unaffected by BSO. Collectively, our in vivo data show that marked depletion of ileal GSH and oxidation of the GSH redox pool does not alter indices of ileal epithelial proliferation or SBR-induced ileal mucosal adaptive growth.

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