1972 Volume 63 Issue 1 Pages 1-10
The present study was undertaken to determine whether the decrease of rat liver RNA by the administration of 4-(dimethylamino)azobenzene (DAB) is brought by the acceleration of the degradation of RNA or by the suppression of RNA synthesis. The half life of 14C-RNA, used as the measure of RNA degradation, was not shortened by the administration of DAB, while RNA polymerase activity of the isolated liver nuclei activated by Mn2+ and (NH4)2SO4 was significantly suppressed. RNA polymerase activity activated by Mg2+ was rather stimulated. A suggestion was also made that DAB prevents newly synthesized RNA from being fixed as the cellular constituents.
A similar observation on liver RNA metabolism was made in the animals in which hepatic carcinogenesis by DAB was inhibited by the concurrent administration of either 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide or 2-amino-5-[2-(5-vitro-2-furyl)-1-(2-furyl)vinyl-1-]-1, 3, 4-oxadiazole. Liver RNA/DNA ratio and Mn2+-(NH4)2SO4-activated RNA polymerase activity were not reduced in these animals. Both RNA polymerase activities and RNA/DNA ratio in the isolated liver nuclei were considerably increased by the concurrent administration of a nitrofuran.
It is concluded that the decrease of liver RNA by the administration of DAB is due to the suppression of the processes of RNA formation, and that the nitrofurans antagonize the action of DAB on liver RNA by increasing the RNA polymerase activity.
