1974 Volume 26 Issue 4 Pages 450-463
In the preceeding paper, it was shown that mammary carcinogenesis with 7,12-DMBA was significantly inhibited by arginine imbalanced diets given to the host, especially when 15% casein diet was supplemented with 5 % arginine. In this paper, to clarify the mechanism responsible for the inhibitory effect of excessive addition of dietary arginine on tumor growth, the influence of arginine treatment on nucleic acid synthesis in tumor tissue was analysed. Experimental animals employed in this series were female Sprague-Dawley rats with mammary carcinoma induced by 7,12-DMBA. Eight m moles/kg of arginine hydrochloride was injected intraperitoneally into rats bearing mammary carcinoma. One hour after the injection of arginine hydrochloride, experimental animals were received intraperitoneal injection of 3H-thymidine-6 or 14C-aspartic acid (U) respectively. Experimental animals were sacrificed either 60 minutes after the injection of 3H-thymidine-6 or 150 minutes after the injection of 14C-aspartic acid (U), and incorporation of radio activity into nucleic acid were analysed.
The following results were obtained:
1. The incorporation of the 14C-aspartic acid (U) into the nucleic acid fraction of liver tissue showed no differences between the arginine treated and control groups, however, the incorporation of 14C-aspartic acid (U) into the nucleic acid fraction of tumor tissue were clearly inhibited in the arginine treated group.
2. The incorporation of 3H-thymidine-6 into the DNA fraction of liver tissue showed no differences between the arginine treated and control groups, whereas the incorpo- ration of 3H-thymidine-6 into the DNA fraction of tumor tissue caused marked inhibition in the arginine treated group. These results suggest that the influence of arginine treatment on nucleic acid syn- thesis in tumor tissue is clearly shown in the salvage pathway instead of the de novo pathway for pyrimidine biosynthesis. teriol.,107,589-591,1971.
