2000 Volume 13 Issue 4 Pages 249-255
To investigate the modifying effects of cinnamaldehyde (CNMA) on the development of lung proliferative lesions, male transgenic mice carrying the human prototype c-Ha-ras gene (rasH2 mice) were given a single intraperitoneal injection of 250 mg/kg urethane (UR) or saline (vehicle control), followed by a diet containing 0.5% CNMA or basal diet, respectively, for 26 weeks. Their non-transgenic CB6F1 littermates (non-Tg mice) were also treated in the same manner. In rasH2 mice, alveolar/bronchiolar hyperplasias were observed in all treated groups including untreated controls, and adenomas were induced in the treated groups except for CNMA-alone group. However, there were no significant intergroup differences in the incidences and multiplicities of these lesions. In addition, although carcinomas were found in both UR-alone and UR+CNMA groups, there was no significant differences in the incidences and multiplicities between them. In non-Tg mice, alveolar/bronchiolar hyperplasias were observed in both untreated control and UR+CNMA groups with no significant differences in the incidences and multiplicities. Adenomas were induced in all treated groups except for CNMA-alone group in non-Tg mice, the incidences and multiplicities were lower than those in rasH2 mice and no significant intergroup differences were observed. There were no significant intergroup differences between UR-alone and UR+CNMA groups in the PCNA labeling indices of adenomas or carcinomas and the areas of adenomas or carcinomas to whole examined area of lungs. The present results suggest that the CNMA treatment under the present experimental conditions does not influence on the development of lung proliferative lesions induced by urethane in both rasH2 mice and non-Tg mice.
