ENDOGENOUS SULFHYDRYLS IN HEALING GASTRIC-MUCOSAL INJURY-INDUCED BY HCL IN THE RAT

Citation
K. Takeuchi et al., ENDOGENOUS SULFHYDRYLS IN HEALING GASTRIC-MUCOSAL INJURY-INDUCED BY HCL IN THE RAT, Digestion, 54(2), 1993, pp. 91-97
Citations number
21
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00122823
Volume
54
Issue
2
Year of publication
1993
Pages
91 - 97
Database
ISI
SICI code
0012-2823(1993)54:2<91:ESIHGI>2.0.ZU;2-O
Abstract
The role of endogenous sulfhydryls (SH) in the heating of HCl-induced gastric injury was investigated in the rat. The animals fasted for 18 h were given 1 ml of 0.6 N HCl by gavage, and they were fed normally f rom 1 h later and killed various days after HCl treatment. Gastric les ions induced by HCl healed to quiescent states within 7 days both macr oscopically and histologically. Mucosal SH levels were markedly reduce d after induction of damage bv HCl, but recovered gradually to or abov e normal values within 5 days. Gastric acidity was also significantly reduced after administration of 0.6 N HCl (induction of lesions), foll owed by a return to normal values within 5 days, although the volume o f gastric contents remained unchanged before and after HCl treatment. The healing of HCl-induced gastric lesions was significantly impaired by diethylmaleate (DEM 0.3 ml/kg X 2) when this drug was given subcuta neously for 5 days. Glutathione (GSH: 100 mg/kg X 2) alone did not aff ect the healing of gastric lesions, but the combined administration of GSH with DEM significantly antagonized the delayed healing caused by DEM. Administration of DEM caused a marked and persistent reduction in the mucosal SH contents, while GSH by itself significantly increased the mucosal SH levels and partially reversed the reduced SH contents c aused bv DEM. Gastric acid secretion was not significantly altered by either DEM or GHS. These results suggest that endogenous SH may play s ome roles in the healing process of gastric mucosal lesions. DEM cause d a deleterious effect on the healing of gastric lesions, probably by reducing the mucosal SH.