Abstract
Recent studies have suggested a central role for alterations in cellular divalent cations in the pathogenesis of red cell damage during in vitro storage [27, 43, 45]. Copper and calcium are known to exchange between plasma and red cells. Passive exchange occurs between plasma free copper and non-erythrocuprein red cell copper, allowing copper to come to equilibrium between plasma and two cellular compartments [4]. Calcium, which enters the red cell by diffusion, is extruded by a process which requires energy [36]. Calcium exodus is mediated by a « pump » which is linked to a calcium-activated ATPase [20, 26, 37, 42, 44, 45, 46]. This phosphohydrolytic enzyme tranduces energy from adenosine triphosphate (ATP) for the work required for calcium extrusion against a steep gradient. Hence, the system in several respects is analogous to the red cell sodium pump [14]. Weed, La Celle and Merrill provided evidence for the physiological importance of the red cell calcium pump by demonstrating that calcium accumulation was accompanied by detrimental changes in biophysical properties of the cell [43]. Studies by Wins and Schoffeniels [45], and Palek, Curby and Lionetti [27, 28] also indicated that calcium ion has an effect on the red cell membrane in vitro, since it induced volume reduction (shrinkage), in part explained as being due to a conformational change in membrane protein.
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Lichtman, M.A., Weed, R.I. (1973). Divalent Cation Content of Normal and ATP-Depleted Erythrocytes and Erythrocyte Membranes. In: Bessis, M., Weed, R.I., Leblond, P.F. (eds) Red Cell Shape. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-88062-9_10
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