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Updated: Aug 12, 2026

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Ex Vivo Intestinal Sacs to Assess Mucosal Permeability in Models of Gastrointestinal Disease
Published on: February 9, 2016
Selenium reduces hemoglobin-induced epithelial damage to intestinal mucosa
Ann L Baldwin1, Elizabeth B Wiley
1Department of Physiology, College of Medicine, University of Arizona, Tucson 85724-5051, USA.
Summary
Selenium (Se) supplementation protected against diaspirin cross-linked hemoglobin (DBBF-Hb) induced epithelial damage in rat intestines. However, Se increased mast cell degranulation, suggesting a protective mechanism independent of mast cells.
Area of Science:
- Biochemistry
- Toxicology
- Gastroenterology
Background:
- Modified hemoglobins, such as diaspirin cross-linked hemoglobin (DBBF-Hb), are investigated as potential blood substitutes.
- Epithelial damage is a concern with blood substitute administration.
- Selenium (Se) is an essential trace element with antioxidant properties.
Purpose of the Study:
- To evaluate if DBBF-Hb causes intestinal epithelial damage.
- To determine if selenium (Se) supplementation mitigates DBBF-Hb-induced epithelial damage.
- To investigate the role of mast cell degranulation in this process.
Main Methods:
- Anesthetized Sprague-Dawley rats were administered DBBF-Hb or control solution (HBS-BSA) after a 3-week selenium (Se) or no-Se pre-treatment.
- Intestinal tissue was examined using light and electron microscopy to assess epithelial integrity (E.I.).
- Mast cell degranulation per villus (MCD) was quantified microscopically.
Main Results:
- DBBF-Hb significantly compromised intestinal epithelial integrity in non-Se rats compared to controls.
- Selenium (Se) pre-treatment prevented DBBF-Hb-induced epithelial damage.
- DBBF-Hb increased mast cell degranulation (MCD) in non-Se rats, but Se supplementation did not reduce this effect and, in fact, increased MCD in both DBBF-Hb and control groups.
Conclusions:
- Diaspirin cross-linked hemoglobin (DBBF-Hb) can induce intestinal epithelial damage.
- Selenium (Se) protects the intestinal mucosal epithelium from DBBF-Hb toxicity.
- The protective mechanism of selenium (Se) against DBBF-Hb-induced damage appears independent of mast cell degranulation.

