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.