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• W2317869812 abstract "145 Increasing attention has been focused on the possible causative role of endogenously generated oxygen-derived species in disorders such as inflammatory bowel disease (IBD). Extracellular glutathione peroxidase (E-GPx) is a glycosylated selenoprotein that reduces hydrogen peroxide, organic hydroperoxides, free fatty acid hydroperoxides and phosphatidylcholine hydroperoxides. All plasma GPx activity is E-GPx and most of it is derived from the kidney. However, the GI tract also synthesizes and secretes E-GPx into the extracellular milieu. We evaluated E-GPx levels in a mouse model of IBD, in which 5 week old male C3N/HeN mice were given drinking water containing 5.0% dextran sodium sulfate (DSS) for 7 days. By day 7, the animals had rectal bleeding associated with intraluminal hemorrhage spanning throughout the cecum, proximal colon, and distal colon. Histological lesions of the cecum, proximal colon and distal colon consisted of multifocal areas of mucosal erosion, reduction in goblet cells, dilated crypts, crypt collapse, submucosal edema, and mixed inflammatory infiltrates of transmural distribution. Plasma E-GPx activity in the DSS-group (0.0464 +/- 0.022 U/mg) was significantly increased compared to the control group (0.0284 +/-0.029 U/mg) (P<0.01). Western blot analysis demonstrated a significant increase (38.3%) in E-GPx protein in the plasma of the DSS-group (P<0.01). E-GPx protein was significantly increased over control in the proximal (78.2%) and distal colon (640.5%) of the DSS-group (P<0.05). Immunohistochemistry studies of the cecum, proximal colon, and distal colon sections of DSS-induced mice demonstrated the presence of E-GPx protein within intact mature absorptive epithelial cells, dilated crypt cells and their extracellular milieu. In comparison, control sections demonstrated localization solely to mature absorptive epithelial cells and its extracellular milieu. After 7 days of DSS treatment, E-GPx mRNA expression relative to tubulin appeared to increase in the cecum, proximal colon, distal colon, and kidney. These results suggest that the increase in E-GPx activity and protein expression in DSS-induced mice may not only be a localized response at the site of injury in the lower GI tract, but may also be a response of the kidneys due to oxidative stress produced in the lower GI tract. This study provides evidence that IBD may be associated with altered local and circulating antioxidant defenses, such as E-GPx." @default.
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• W2317869812 date "1999-10-01" @default.
• W2317869812 modified "2023-09-25" @default.
• W2317869812 title "ALTERED EXPRESSION OF EXTRACELLULAR GLUTATHIONE PEROXIDASE IN MICE WITH DEXTRAN SODIUM SULFATE-INDUCED EXPERIMENTAL COLITIS" @default.
• W2317869812 doi "https://doi.org/10.1097/00005176-199910000-00171" @default.
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