1. In rats with acute turpentine-induced inflammation, there was a reduced reutilization of radioiron from transfused senescent erythrocytes but a normal utilization of transferrin-bound Fe59 after a 40-hour period. There was a pronounced retention of tracer from the nonviable red cells by the livers and spleens of the inflamed animals.

2. During inflammation, the plasma iron turnover fell by about 50 per cent, while the fraction of plasma iron removed per hour was increased. However, there was no marked change in the relative distribution of transferrin-bound Fe59 to the liver, spleen and bone marrow (after perfusion). Transferrin-bound Fe59 initially appeared at an increased rate in the circulating red cell mass.

3. Following administration of ferric ammonium citrate in order to raise the plasma iron level, there was a rise in the plasma iron turnover of the inflamed rats, in contrast to the control animals. Diversion of radioiron to the liver and spleen was not markedly increased under these conditions.

4. It is concluded that the immediate fall in plasma iron turnover and hypoferremia during acute turpentine inflammation results mainly from an inhibition of the release of iron derived from senescent red cells into the plasma. An increased avidity of the liver, and of marrow red cell precursors and/or reticulocytes for plasma iron may accentuate the fall in plasma iron levels. There appeared to be no inhibition of the bone marrow capacity to turn over larger amounts of plasma iron during inflammation. These results may help in the interpretation of disturbances of iron metabolism during the acute inflammatory state.

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