caa a22 4500 465764045 CHVBK 20180323111908.0 cr unu---uuuuu 170327e19901201xx s 000 0 eng 10.1007/BF00916370 doi (NATIONALLICENCE)springer-10.1007/BF00916370 Oxidant defense mechanisms in the human colon [Elektronische Daten] [Matthew Grisham, Richard MacDermott, Edwin Deitch] Reactive oxygen metabolites have been implicated as important mediators of inflammation-induced intestinal injury associated with ischemia (and reperfusion), radiation, and inflammatory bowel disease. Because the colonie mucosa may be subjected to significant oxidant stress during times of acute and chronic inflammation, knowledge of the oxidant defense mechanisms in the colon is of biologic and potential clinical importance. Therefore, the objective of this study was to quantify the specific activities of superoxide dismutase (SOD), catalase, and GSH peroxidase in the normal human colon. We found low, but significant, amounts of all three enzymes in the mucosa, submucosa, and muscularis/serosa of the human colon. However, the mucosal levels of SOD (3.6±0.3 units/mg protein), catalase (11±3 units/ mg), and GSH peroxidase (15.2±0.8 mU/mg) represented only 8%, 4%, and 40%, respectively, of those values determined for human liver. Colonic epithelial cells derived from mucosal biopsies exhibited significantly higher specific activities for SOD (12±0.5 units/mg) and catalase (26±6 units/mg) when compared to whole mucosa, suggesting most of the mucosal activity was associated with the epithelial cells and not the lamina propria. In a comparative study, we found that a human colonic carcinoma cell line (CaCo-2) contained significantly lower SOD (6 ±0.5 units/mg) and catalase (6±0.6 units/mg) activities when compared to colonic epithelial cells. Taken together, our data suggest that: (1) the colonic mucosa is relatively deficient in antioxidant enzymes when compared to liver, and (2) most of the protective enzyme activity is localized within the epithelium and not the mucosal interstitium. Plenum Publishing Corporation, 1990 Grisham Matthew Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport, Louisiana aut MacDermott Richard Gastroenterology Section, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania aut Deitch Edwin Department of Surgery, Louisiana State University Medical Center, Shreveport, Louisiana aut Inflammation Kluwer Academic Publishers-Plenum Publishers 14/6(1990-12-01), 669-680 0360-3997 14:6<669 1990 14 10753 https://doi.org/10.1007/BF00916370 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00916370 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Grisham Matthew Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport, Louisiana aut NATIONALLICENCE 700 1- MacDermott Richard Gastroenterology Section, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania aut NATIONALLICENCE 700 1- Deitch Edwin Department of Surgery, Louisiana State University Medical Center, Shreveport, Louisiana aut NATIONALLICENCE 773 0- Inflammation Kluwer Academic Publishers-Plenum Publishers 14/6(1990-12-01), 669-680 0360-3997 14:6<669 1990 14 10753 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer