Chemically induced colonic carcinomas in rats have several features similar to human neoplasm. In the present study, 60 male Sprague-Dawley rats were injected s.c. once a week for 12 weeks with 21 mg/kg body weight of 1,2-dimethylhydrazine dihydrochloride. As controls, 15 rats were injected s.c. with 1 mi of EDTA solution during the same period. Tissue specimens from the colon from four groups of animals, 10 in each, namely rats without tumour, with dysplasia and lymphoid hyperplasia, with colonic adenocarcinoma, and controls were investigated. The concentrations of seven neuroendocrine peptides known to occur in the colon were determined in tissue extracts by radioimmunoassay. The concentrations of somatostatin, neurotensin, substance P and galanin were significantly higher in the colon of rats with lymphoid hyperplasia and dysplasia and with adenocarcinoma than in controls. There was no statistical difference between controls and rats without colonic changes regarding the concentrations of somatostatin, substance P, neurotensin and galanin. The colonic levels of PYY, NPY and VIP in treated rats did not differ significantly from those of controls. The present observations support the assumption that neuroendocrine peptides are involved in the pathogenesis of colorectal carcinoma. Moreover, the changes in the colonic neuroendocrine peptides in this animal model differed from those found in human patients with colorectal carcinoma, possibly due to differences in species and/or to age. Whereas the increased levels of somatostatin and galanin in rats might be a way for the body to defend itself against the tumour invasion, the increase in neurotensin levels may be one of the factors promoting tumour growth. The increased concentration of substance P could be a part of the immune response to the tumour.
