Flatman P W
Department of Physiology, University Medical School, Edinburgh, Scotland.
Magnes Res. 1988 Jul;1(1-2):5-11.
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.
尽管存在内向的镁电化学梯度，但随着红细胞的老化，其细胞内镁浓度会下降。这种下降是由钠依赖性镁转运引起的，而钠依赖性镁转运依赖于细胞代谢。在具有正常细胞年龄分布的悬浮液中，人体红细胞中的镁以平均约4微摩尔/升细胞/小时的速率流失。年轻细胞可能比衰老细胞流失镁的速度更快，这可能是因为它们的细胞内游离镁浓度更高。这会影响镁转运的激活，而镁转运对细胞内镁浓度有强烈的依赖性。该转运体是一种钠-镁反向转运体，它可能从钠梯度中获取部分（如果不是全部）能量来克服任何相反的镁电化学梯度。转运可能受蛋白质磷酸化调节，或者可能需要代谢能量的输入，也许来自ATP的水解，并且会被高浓度的氨氯吡脒抑制。除了对细胞镁浓度的这种长期控制外，由于细胞质镁缓冲特性的变化还会出现波动。例如，脱氧会导致游离镁浓度增加，这会改变细胞内的代谢和转运。因此，红细胞内游离镁的浓度并非恒定不变，而是随着细胞循环而持续振荡。
