トランスフェリンの代謝と機能

DOI Web Site

書誌事項

タイトル別名
  • Metabolism and Function of Transferrin
  • トランスフェリン ノ タイシャ ト キノウ

この論文をさがす

抄録

1) Transferrin was determined immunochemically with the anti-human transferrin rabbit serum, which precipitated specifically transferrin as demonstrated by Ouchterlony's double diffusion method and immunoelectrophoresis. A linear relationship was found to exist between the immunochemically determined transferrin level and the chemically estimated TIBC in various diseases. In 87 cases of clinical cases, the ratio of TIBC to immunochemically determined transferrin level was 1.29±0.028 μg of iron per milligram of transferrin. Hypertransferrinemia was observed in iron deficiency anemia (essential hypochromic anemia, agastric iron deficiency anemia, peptic ulcer with occult bleeding, hook worm anemia), Banti's syndrome with hyposideremia and acute hepatitis. Hypotransferrinemia was found in liver cirrhosis, nephrotic syndrome, gastric cancer, rheumatoid arthritis and chronic granulocytic leukemia. In 17 cases of liver diseases, the serum transferrin level correlated most significantly with serum albumin fraction. Those with positive turbidity tests (TTT, ZST, Takata) showed significantly low serum transferrin level as compared with those with negative reaction. Based on these findings, the hepatic origin of transferrin was presumed. Transferrin excreted in the urine of 6 cases of chronic nephritis was determined immunochemically and was proved to comprise 4.1 (2.2 to 6.9) percent of the total urine protein.<br>2) The turnover rate of human transferrin was investigated by following the disappearance of intravenously administered iodinelabelled transferrin in normal subjects and patients suffered from various diseases. In 4 normal subjects the following mean and range values were obtained.<br>Half time 11.0 days (10.5∼12.1)<br>Transferrin turnover rate 6.3 percent/day (5.7∼6.6)<br>19.6 mg/day/kg (15.9∼23.3)<br>In the cases of essential hypochromic anemia was observed a longer half-time and a greater exchangeable pool than those of normal controls, but the cases of iron deficiency anemia with slight gastrointestinal bleeding showed a shorter half-time than that of essential hypochromic anemia. In the cases of liver cirrhosis, the serum transferrin and exchangeable pool were decreased. but the half-time was normal. In the cases of chronic nephritis (nephrotic form), the half-time was short and the exchangeable transferrin pool was small as compared with those of the normals.<br>3) Rat transferrin was isolated using rivanol and column chromatography on ion exchange cellulose. Anti-rat transferrin rabbit sera were prepared and they reacted specifically with the rat transferrin as shown by immunoelectrophoresis. The transferrin formation was demonstrated by determining the incorporation of glycine-2-C14 into the transferrin fraction of supernatant of liver slices in vitro. The quantity of the glycine incorporation was 1.7±1.17 (10-3 μM/mg-protein/hr) in normal rat liver. The incorporation of glycine-2-C14 into the transferrin of spleen supernatant was negligibly small. In iron deficient rats with hypertransferrinemia, was observed a higher incorporation into the transferrin of liver supernatant, while in cirrhotic liver with hypotransferrinemia the incorporation was lower than that of normal controls. Based on these results, it would be reasonable to presume the increase of transferrin formation in iron deficient and the decrease of that in cirrhotic liver.

収録刊行物

  • 臨床血液

    臨床血液 5 (Suppl.), S98-S107, 1964

    一般社団法人 日本血液学会

詳細情報 詳細情報について

問題の指摘

ページトップへ