Transglutaminase in response to hypertonic NaCl-induced gastric mucosal injury in rats.
BACKGROUND: Polyamines serve as substitutes for transglutaminase-catalyzed protein cross-linking and are essential to the healing of gastric mucosal lesions. This study determines whether transglutaminase and protein cross-linking have a role in the healing of hypertonic NaCl-induced gastric lesions. METHODS: Rats were fasted 22 hours before given 1 mL 3.4 Mol/L NaCl intragastrically. Gastric mucosa was examined histologically and grossly, and transglutaminase activity was measured as the Ca(2+)-dependent covalent incorporation of [3H]putrescine into acid-precipitable protein. RESULTS: Transglutaminase activity increased significantly from 2 to 8 hours, peaking between 4 and 6 hours after NaCl administration. Lesions were significantly produced after 2 hours, and damage paralleled transglutaminase activity. Dansylcadaverine (200 mg/kg orally), a specific inhibitor of protein cross-linking, prevented the increases in transglutaminase activity and significantly delayed healing but had no effect on lesion formation. CONCLUSIONS: These results indicate that (1) hypertonic NaCl-induced gastric mucosal damage is associated with a significant increase in transglutaminase activity and (2) increased transglutaminase activity is involved in the mechanism of normal mucosal healing.[1]References
- Transglutaminase in response to hypertonic NaCl-induced gastric mucosal injury in rats. Wang, J.Y., Viar, M.J., Johnson, L.R. Gastroenterology (1993) [Pubmed]
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