Compound 48/80 and substance P induced release of histamine and serotonin from rat peritoneal mast cells

Abstract

The effect of substance P and compound 48/80 on histamine and serotonin release from not isolated and isolated mast cells have been compared in experiments in vitro. The response of not isolated and isolated mast cells were virtually identical. The release of both amines, in response to 48/80 and substance P, was dose-dependent. The percentage of histamine released by 48/80 was significantly higher than the percentage of serotonin, the difference being higher at lower concentrations of compound 48/80 after 15 min of incubation. Substance P also showed a tendency to higher efficiency for histamine than for serotonin release. In contrast to 48/80, the dose-response curves for histamine and serotonin release were parallel. These results support the view that the ratio between histamine and serotonin release depends on the liberator used. They also showed that this ratio can depend on the concentration of the agent inducing secretion. The results indicate that substance P as well as 48/80 act rather selectively as histamine liberators and that there is some difference in releasing properties of 48/80 and substance P.

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).…”

Release of 5‐hydroxytryptamine, dopamine and noradrenaline in the rat vas deferens in the presence of compound 48/80, veratridine or K+

“…Compound 48/80, which is known to induce the release of 5-HT and histamine from mast cells (Moran et al, 1962;Irman-Florjanc & Erjavec, 1983;Koibuchi et al, 1985), caused a rapid and pronounced overflow of 5-HT from the rat isolated vas deferens (Figures 1 and 2). This finding indicates that a considerable part of the amine in this organ is stored in mast cells, as previously suggested by Fuenmayor et al (1976).…”

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

“…The stomachs were then opened along the greater curvature and examined for lesions in the glandular part under a dissecting microscope (ϫ10). The severity of gastric mucosal lesions was estimated using the index of the following eight grades of lesions as described in our previous reports [3][4][5]13,14) : grade 0, no lesion (normal); grade I, edema only; grade II, damaged area of 1-10 mm 2 Administration of Vitamin E or SOD Plus CAT Vitamin E (RRR-a-Toc.) (50, 100 or 250 mg/kg), dissolved in 5% Tween 80, was orally administered to rats treated with and without C48/80 at a constant dosing volume of 5 ml/kg BW with a stomach tube.…”

“…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.…”