Abstract
Abstract
The influence of oral sodium salicylate (NaSal) or ethanol (ETOH) on glucosamine synthetase (GmS) specific activity in rat fundic and antral mucosae and liver was measured. Sodium salicylate, 32 mg/kg in 0.1 N HCl, caused a 46% decrease in GmS specific activity in only 5 min. Recovery to 179% of control was complete by 30 min. Larger doses of Nasal caused more severe damage to the gastric mucosa and more persistent decreases in fundic GmS specific activity and also decreased liver GmS activity. ETOH, 20% (v:v) in 0.1 N HCI, 1.6 g/kg, caused a 29% decrease in GmS activity in the fundic mucosa in 15 min. Recovery, to 157% of control was complete in 30 min. We conclude that specific inhibition of hexosamine synthesis, not attributable to necrosis or general metabolic decline occurs during Nasal- and ETOH-induced gastric damage and may be involved jointly with acid not only in the development but also in the delayed healing of severe damage.
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