A change in gastric mucosal ascorbic acid status with the formation, progression, and recovery of compound 48/80-induced acute gastric mucosal lesions in rats.

We examined whether gastric mucosal ascorbic acid status changes with the formation, progression, and recovery of acute gastric mucosal lesions in rats treated with compound 48/80, a mast cell degranulator. Fasted Wistar rats received a single intraperitoneal injection of compound 48/80 (0.75 mg/kg). Apparent gastric mucosal lesions occurred 0.5 h after compound 48/80 treatment, progressed gastric mucosal lesions were observed at 3 h, and a partial recovery of the progressed lesions was found at 6 h. The gastric mucosal concentrations of total and reduced ascorbic acids in compound 48/80-treated rats decreased to approximately 60% of the levels of untreated rats at 3 h after the treatment but the decreased concentrations of total and reduced ascorbic acids were almost completely returned to the levels of untreated rats at 6 h. The gastric mucosal concentration of oxidized ascorbic acid in compound 48/80-treated rats showed little change. The serum concentrations of total and reduced ascorbic acids in compound 48/80-treated rats increased at 0.5 h after the treatment and further increased at 3 h but the increased concentrations of total and reduced ascorbic acids were almost completely returned to the levels of untreated rats at 6 h. The serum concentration of oxidized ascorbic acid in compound 48/80-treated rats increased transiently at 0.5 h after the treatment. The hepatic concentrations of total. reduced, and oxidized ascorbic acids in compound 48/80-treated rats increased 3 h after the treatment, but these increases were not observed at 6 h. These results indicate that gastric mucosal ascorbic acid status is disrupted with the progression of acute gastric mucosal lesions in rats treated with compound 48/80.