5/21/2023 0 Comments Cell turnover![]() ![]() The measurement of carbon monoxide (CO) production was formerly very tedious, requiring elaborate rebreathing apparatus. There are too many variables that affect the serum bilirubin level to make it a reliable, quantitative measurement of red cell destruction. 40 Both of these compounds are derived almost exclusively from catabolized hemoglobin and measurements of their rate of production have provided useful information about the red cell life span. ![]() There are two approaches to the calculation of the red cell life span by indirect methods: from a measurement of the rate of production of red cells using radioactive iron and from a measurement of the rate of breakdown of heme to bilirubin, 39 that is, the release of carbon monoxide from catabolized heme. Although computer-assisted methods can resolve ambiguities, the inherent biologic and technical variations in measuring red cell life span are such that it is better to rely on chromium T 1/2 with intuitive adjustments based on clinical findings. 30 Furthermore, the best fit of data is rarely linear or exponential, but somewhere between. One objection to this method is that the degree of chromium elution is not a constant but varies from day to day and is influenced by various disease states. If the data indicate exponential disappearance and it is necessary to use a semilogarithmic paper in order to depict the data on a straight line, the destruction is random and the life span is 1.44 times the half-life. 35 If the data lie on a straight line, the destruction is by senescence and the life span can be calculated as twice the half-life. 11, 12 All of these changes have been investigated as signals for recognition by the macrophages.īecause merely expressing the red cell life span measured by chromium as chromium T 1/2 will not give information as to the character of destruction, senescence versus random, it has been recommended that in addition a correction factor for chromium elution be used and the data recorded using linear coordinates. 46), 9 a decrease in deformability as the result of increased oxidative stress, 10 and an increase in cell surface-bound immunoglobulins and complement components ( Chap. 1, 2 These include a decrease in the activity of enzymes, 3 a progressive decrease of ATP content, 4 a loss of lipid asymmetry with exposure of phosphatidylserine, 5 an accumulation of lipid peroxidation products, 6 a desialylation of membrane glycoprotein, 7 an exposure of cryptic senescent antigens, 8 aggregation of band 3 protein ( Chap. As red blood cells age, several physiologic changes occur that may serve as signals for recognition by macrophages. The precise molecular mechanism by which macrophages recognize senescent red blood cells for phagocytosis remains largely unknown. This is an extremely efficient process as macrophages phagocytose approximately 5 million erythrocytes every second without a significant release of hemoglobin into the circulation. Normal human red blood cells have a life span of approximately 120 days, after which they are engulfed by macrophages. Candidates for such changes include changes in membrane band 3 and exposure of phosphatidylserine on the membrane, which may be of major importance. This has made the senescent changes in the red cell that mark it for destruction difficult to study. Thus, cell density is not a good marker for aged red cells. The mitochondrial and ribosomal removal highlighting maturation of the reticulocyte is accompanied by increasing cell density, but after a few days of intravascular life span there is little further increase in density or other changes in the physical property of the red cells. Such studies show that normal human red cells have a finite life span averaging 120 days, with very little random destruction. The survival of red cells in the circulation can be measured in a variety of ways: (1) by labeling with radioactive isotopes, particularly chromium-51 ( 51Cr), and assessing the disappearance of the radioactive tag from the circulation over time (2) by labeling the erythrocytes with biotin or a fluorescent dye and measuring this marker over time (3) by determining the disappearance of transfused antigen-matched allogeneic erythrocytes using immunologic markers and (4) by measuring the excretion of carbon monoxide, a product of heme catabolism.
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