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Impairment of intestinal mucosal antioxidant defense system during Salmonella typhimurium infection
The mucosal pathology of Salmonella typhimurium infection may in part be due to the excessive production of reactive oxygen species (ROS). The influence of S. typhimurium infection on the intestinal mucosal antioxidant defense system was investigated. We injected ligated rat ileal loops with Salmone...
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Published in: | Digestive diseases and sciences 1998-03, Vol.43 (3), p.646-651 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | The mucosal pathology of Salmonella typhimurium infection may in part be due to the excessive production of reactive oxygen species (ROS). The influence of S. typhimurium infection on the intestinal mucosal antioxidant defense system was investigated. We injected ligated rat ileal loops with Salmonella live culture or toxin. After 18 hr of infection, the animals were killed and enterocytes isolated from the ileal loops. The enterocyte-reduced glutathione (GSH) content and activities of the enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase, glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH) were spectrophotometrically estimated. The vitamin E and A contents were determined by high-performance liquid chromatography (HPLC). In both the Salmonella live culture and toxin-treated groups, the enterocyte GSH and vitamin E contents and activities of the enzymes SOD, GSH-Px, catalase, GR, and G6PDH were significantly decreased as compared to the control group. However there was a significant increase in the enterocyte activity of GST. There was no change in the vitamin A content of the enterocytes. These findings might indicate a decreased endogenous intestinal protection against ROS in S. typhimurium-mediated infection, which could contribute to the pathogenesis of the disease. |
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ISSN: | 0163-2116 1573-2568 |
DOI: | 10.1023/A:1018887813713 |