Subcutaneous injection of 3 mg benzo[a]pyrene into the right hind leg of experimental rats resulted in local tumors in the area of application in all the animals. The same dose of disodium cromoglycate applied prior to benzo[a]pyrene prevented tumor formation or provoked a significant inhibition of the carcinogenic process, e.g. delay of tumor formation and of a reduced size, a number of mitoses and cytological abnormalities and a prolongation of the animal's life. In the in vitro Salmonella typhimurium mutation assay of Ames, disodium cromoglycate eliminated toxicity and mutagenicity of 5-nitro-2-furylacrylic acid. The results would suggest that the initial response of the cell to benzo[a]pyrene had been conducted through the calcium-dependent exocytic pathway, which can be efficiently blocked by disodium cromoglycate, probably by preventing the signals increase in free intracellular calcium concentration. The preserved calcium balance as a consequence of the effect of disodium cromoglycate on benzo[a]pyrene-induced cell response might be a factor responsible for the carcinogenesis inhibition phenomena. The results of the in vitro study in correlation with those obtained in vivo support the suggestion that disodium cromoglycate may influence parallel structures in various cell types.
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