title: Endogenous sulfhydryls in healing gastric mucosal injury induced by HCl in the rat.
abstract: The role of endogenous sulfhydryls (SH) in the healing 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 from 1 h later and killed various days after HCl treatment. Gastric lesions induced by HCl healed to quiescent states within 7 days both macroscopically and histologically. Mucosal SH levels were markedly reduced after induction of damage by HCl, but recovered gradually to or above normal values within 5 days. Gastric acidity was also significantly reduced after administration of 0.6 N HCl (induction of lesions), followed by a return to normal values within 5 days, although the volume of 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 subcutaneously for 5 days. Glutathione (GSH: 100 mg/kg x 2) alone did not affect 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 caused by DEM. Gastric acid secretion was not significantly altered by either DEM or GHS. These results suggest that endogenous SH may play some roles in the healing process of gastric mucosal lesions. DEM caused a deleterious effect on the healing of gastric lesions, probably by reducing the mucosal SH.
authors.affiliation: Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Takeuchi
authors.forename: M
authors.initials: M
authors.lastname: Okada
authors.forename: K
authors.initials: K
authors.lastname: Ueshima
authors.forename: T
authors.initials: T
authors.lastname: Ohuchi
authors.forename: S
authors.initials: S
authors.lastname: Okabe
mesh_terms: D000818:Animals; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000502:physiology; D005978:Glutathione / Q000494:pharmacology; D006851:Hydrochloric Acid; D008297:Male; D008298:Maleates / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013438:Sulfhydryl Compounds / Q000502:physiology*; D013997:Time Factors; D014945:Wound Healing / Q000502:physiology*
chemical_list: D008298:Maleates; D013438:Sulfhydryl Compounds; C014476:diethyl maleate; D005978:Glutathione; D006851:Hydrochloric Acid