Experiments uncover changes in hepatic ferritin levels in tumor-bearing rats, indicating metabolic differences.
In the present experiments the method of isolation of hepatic ferritin first proposed by Drysdale and Munro was investigeted and the validity of using this method for the quantitative determination of hepatic ferritin was confirmed by the recovery and reproducibility experiments. With this method synthetic studies of hepatic ferritin were undertaken in tumor bearing rats as well as in normal controls to elucidate the characteristic features of hepatic ferritin synthesis of tumor bearing rats. The results were summarized as follows : 1) The final isolated ferritin was shown to be sufficiently pure as revealed by polyacrylamide gel electrophoresis and immunoelectrophoresis. 2) The method of isolation of hepatic ferritin was modified in the following two points. The first is the utilization of the final isolated ferritin for the quantitative determination of hepatic ferritin based on recovery and reproducibility experiments. The second is an additional procedure of precipitation of the Sephadex G-200 column fraction by half saturation with ammonium sulfate, which gave a favourable concentration of the final isolated ferritin for its determination. 3) The method of isolating hepatic ferritin was investigated and the recovery of the final isolated ferritin was 78.3~7.3 per cent. Since the reproducibility was fair within a range of 11.3 per cent of the coefficient of variation, this method was regarded as valid for the quantitative determination of hepatic ferritin. 4) The hepatic ferritin content of the liver was markedly reduced in both iron and protein in tumor bearing rats and in bled rats. Both hepatic ferritin iron and protein increased in rats treated with intraperitoneal injections of iron and in rats with turpentine oil abscess. 5) Iron administration to normal rats caused a more than ten fold acceleration of 14C-leucine incorporation into hepatic ferritin, while incorporation of the labeled aminoo acid into the total liver protein was not accelerated by iron administration. The amount of hepatic ferritin increased to four fold of the initial level. 6) In tumor bearing rats a low net increase in hepatic ferritin in response to 14C-leucine incorporation was noted when compared with that of normal controls. This discrepancy might be explained by the difference in the amino acid pool to be utilized for ferritin synthesis. 7) Degradation of hepatic ferritin which occured rapidly in tumor bearing rats was found to be the cause of the low net increase in hepatic ferritin especially after 7 hours of iron administration.
No takes yet. Share an insight, caveat, or question.
Matsuda Mikihito (1969) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: