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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.

journal of nutritional science and vitaminology

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