Ultrastructure of mucosal mast cells in normal and compound 48/80-treated rats

Protective Effect of Teprenone Against Acute Gastric Mucosal Lesions Induced by Compound 48/80, a Mast Cell Degranulator, in Rats

“…Compound 48 / 80 is known to cause degranulation of connective tissue mast cells, but not mucosal mast cells, with release of serotonin and histamine from the cells (19,20). We have shown in rats with a single treatment of compound 48 / 80 that the development of gastric mucosal lesions occurs with decreases in Se-glutathione peroxidase activity and vitamin E and hexosamine contents and increases in neutrophil infiltration, xanthine oxidase (XO) activity, and lipid peroxide content in the gastric mucosal tissue and that gastric mucosal blood flow is reduced with gastric mucosal lesion formation, while the decreased blood flow is recovered with the lesion progression (21).…”

Structure, specificity and localization of the serine proteases of connective tissue

“…Kitamura et al [54] have shown that atypical mast cells of mouse small intestine, but not normal mast cells, arise from precursor cells derived from bone marrow. These observations, together with the morphologic [55] and histologic [56] differences between atypical and normal mast cells strongly suggest that the cells are distinct types.…”

Effect of Oral Vitamin E Administration on Acute Gastric Mucosal Lesion Progression in Rats Treated with Compound 48/80, a Mast Cell Degranulator

“…1,2) We have shown in rats with a single C48/80 treatment that the development of gastric mucosal lesions occurs with decreases in Se-glutathione peroxidase (Se-GSHpx) activity and vitamin E and hexosamine levels and increases in neutrophil infiltration, xanthine oxidase (XO) activity, and lipid peroxide level in the gastric mucosal tissue and that gastric mucosal blood flow changes like ischemia-reperfusion during gastric mucosal lesion development.3) We have also shown in rats treated once with C48/80 that neutrophils infiltrating into the gastric mucosal tissue participate in gastric mucosal lesion formation and progression, while the xanthine-XO system in the gastric mucosal tissue takes part mainly in the lesion progression. 4) Furthermore, it has been shown in rats treated once with C48/80 that acutely released endogenous serotonin contributes to gastric mucosal lesion formation, while released endogenous histamine mainly contributes to the lesion progression, although gastric acid plays no important role in the pathogenesis of the C48/80-induced gastric mucosal lesion.…”

“…1,2) We have shown in rats with a single C48/80 treatment that the development of gastric mucosal lesions occurs with decreases in Se-glutathione peroxidase (Se-GSHpx) activity and vitamin E and hexosamine levels and increases in neutrophil infiltration, xanthine oxidase (XO) activity, and lipid peroxide level in the gastric mucosal tissue and that gastric mucosal blood flow changes like ischemia-reperfusion during gastric mucosal lesion development.…”