The control of red cell magnesium

Abstract

Red cell magnesium concentration falls as cells age in spite of an inwardly directed magnesium electrochemical gradient. This fall is brought about by sodium-dependent magnesium transport, which depends on cell metabolism. Magnesium is lost from human red cells, in a suspension with a normal age distribution of cells, at an average rate of about 4 mumol/litre cell/h. Young cells probably lose magnesium faster than old cells, possibly because their intracellular ionized magnesium concentration is higher. This affects the activation of magnesium transport, which has a steep dependence on intracellular magnesium concentration. The transporter is a sodium-magnesium antiport which may obtain from the sodium gradient some, if not all, the energy to overcome any opposing magnesium electrochemical gradient. Transport may be regulated by protein phosphorylation or may require input of metabolic energy, perhaps from the hydrolysis of ATP, and is inhibited by high concentrations of amiloride. Superimposed on this long-term control of cell magnesium concentration are fluctuations due to changes in the magnesium buffering characteristics of the cytoplasm. For instance, deoxygenation results in an increase in free magnesium concentration which can alter metabolism and transport in the cell. The concentration of ionized magnesium inside red cells is not therefore constant, but continually oscillates as the cells circulate.