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Research Article Free access | 10.1172/JCI106302

Hemolysis of “stress” reticulocytes: a source of erythropoietic bilirubin formation

Stephen H. Robinson and Maria Tsong

Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215

Find articles by Robinson, S. in: PubMed | Google Scholar

Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215

Find articles by Tsong, M. in: PubMed | Google Scholar

Published May 1, 1970 - More info

Published in Volume 49, Issue 5 on May 1, 1970
J Clin Invest. 1970;49(5):1025–1034. https://doi.org/10.1172/JCI106302.
© 1970 The American Society for Clinical Investigation
Published May 1, 1970 - Version history
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Abstract

The formation of bilirubin-14C was measured in rats given transfusions of red blood cells containing 14C-labeled hemoglobin heme. Per cent conversion of hemoglobin-14C to bilirubin was 4 times greater with transfusion of “stress” reticulocytes from rats responding to hemorrhage than with normal reticulocytes from unstimulated donors. When the increased number of labeled reticulocytes produced by hemorrhaged donors was also considered, the total magnitude of labeled bilirubin formation was almost 20 times higher with stress as compared to normal reticulocytes. The findings were not influenced by splenectomy of either donor or recipient rats, iron loading of donors, or bleeding of recipients. However, bilirubin-14C formation fell off progressively as studies were performed at longer intervals after erythroid stimulation.

Total bilirubin-14C formation in rats transfused with stress reticulocytes was compared to the production of early-labeled bilirubin from all potential sources in intact rats bled according to the same schedule used in the transfusion experiments. It is estimated that degradation of hemoglobin from sress reticulocytes accounts for virtually the entire rise in erythropoietic bilirubin formation from 24 to 96 hr after glycine-2-14C administration, but that additional sources make a major contribution before that time. These findings are consistent with the concept that destruction of immature erythroid cells in the peripheral blood, and probably in the bone marrow, accompanies the physiologic response to erythroid stimulation.

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