L-glutamine enemas attenuate mucosal injury in experimental colitis.

PURPOSE: The aim of this study was to investigate the role of 1-glutamine, short chain fatty acid, prednisolone, and mesalazine (5-aminosalicylic acid) enemas on mucosal damage and inflammation in experimental colitis. METHODS: Colitis was induced in rats with trinitrobenzene sulfonic acid in ethanol. Saline (n = 14), prednisolone (n = 13), 5-aminosalicylic acid (n = 14), 1-glutamine (n = 14), and short chain fatty acid (n = 13) enemas were applied twice daily to the rats for seven days after the induction of colitis. The sham group (n = 9) received only saline enemas. Rats were killed at the seventh day and their colonic macroscopic inflammatory scores were determined. Colonic mucosal gamma glutamyl transpeptidase activity and colonic mucosal malondialdehyde levels were measured. The same measurements but no enemas were done in the control group (n = 7). RESULTS: There were significant differences in macroscopic inflammatory scores between sham and colitis groups (P < 0.001). The macroscopic inflammatory scores of the colitis group were higher than the short chain fatty acid and glutamine groups (P < 0.05). Whereas the mucosal gamma glutamyl transpeptidase activity was diminished in prednisolone, 5-aminosalicylic acid, and short chain fatty acid groups when compared with the control group; in the colitis, sham, and glutamine groups the activity of this enzyme did not change. The mucosal malondialdehyde levels were significantly lower in the prednisolone and glutamine groups than in the colitis group. CONCLUSION: Only one of four agents tested, namely, 1-glutamine enemas, could decrease the severity of colitis both morphologically and biochemically. Moreover, L-glutamine prevented the colitis-induced oxidant injury in the colonic mucosa. On the other hand, prednisolone and short chain fatty acids seemed to improve only the physiologic changes of colitis.

Prostaglandin synthetase inhibition reduces peritonitis-induced early liver oxidant stress.

This study was undertaken to determine whether or not the prostanoid metabolism contributes to peritonitis-induced early liver oxidant stress. Lipid peroxidation products, malondialdehyde (MDA) and conjugated dienes (CD), were used to monitor oxidant stress. The rats were given a 5-cc intraperitoneal (i.p.) injection of 25% rat feces suspension and then received either i.p. saline (peritonitis group, n = 11), vitamin E (n = 6), or diclofenac (n = 6). The liver and plasma MDA and CD levels were measured after 3 h. The plasma and liver MDA and CD levels were significantly higher in the peritonitis group than in the control (n = 9). Prostaglandin synthetase inhibitor (diclofenac) kept the liver and plasma MDA and CD at control levels. Antioxidant alpha tacopherol (vitamin E) was thus found not to be effective in reducing these increased MDA and CD levels. Peritonitis-induced early oxidant stress in the liver seems to be mediated by the oxidant-independent activation of the cyclooxygenase pathway.

Effects of vitamin E and cimetidine on peritonitis-induced lipid peroxidation.

To investigate the effects of acute fecal peritonitis on plasma and tissue lipid peroxidation and possible protective effects of vitamin E (Vit E) and cimetidine at 4 h in a rat peritonitis model, four groups were designated as: controls, peritonitis, Vit E and cimetidine. Plasma, liver, lung and kidney thiobarbituric acid reactive substances (TBARS) and conjugated diene (CD) levels were measured to monitor oxidative injury. The present fecal peritonitis model caused a significant elevation in liver TBARS; however, neither Vit E nor cimetidine was effective in preventing TBARS formation. Administration of Vit E and cimetidine caused significant decrements from the peritonitis value in liver and lung CD levels.