Transport of magnesium across biological membranes
- PMID: 2130822
Transport of magnesium across biological membranes
Abstract
The movement of Mg across biological membranes is reviewed from the perspectives of (1) passive transport, (2) primary active transport and (3) secondary active transport. Since all cells maintain intracellular Mg2+ at a lower electrochemical potential than extracellular Mg2+, active transport pumps bringing Mg2+ into the cell have neither been postulated nor been confirmed. Most evidence points to influx leaks, presumably via membrane channels and carriers which do not perfectly exclude Mg2+. However, Mg2+ currents have been measured in prokaryotic and eukaryotic cells suggesting the presence of Mg2+ channels. Mg2+ influx through channels is largely driven by the membrane voltage because transmembrane Mg2+ concentration differences are not very large. Efflux mechanisms have attracted most of the investigative focus. Secondary active transport by way of Na/Mg exchange appears to be widely distributed in eukaryotic cells. The early investigations of Na/Mg exchange had Mg2+ efflux driven solely by the Na+ influx (secondary active transport). However, recent studies have revealed an ATP dependence of Na/Mg exchange which may reflect the operation of an Mg2+ pump (primary active transport). Similar mechanisms of Mg2+ influx and efflux appear to operate in epithelial tissues which may net absorb or secrete Mg2+. In recent years, the intact red blood cell has emerged as the model of choice for studies of Mg2+ membrane transport. However, further probing of the details of individual transport mechanisms may be complicated by the presence of multiple parallel Mg2+ influx and efflux systems in intact cells. Accordingly, it would appear that the next round of advances in membrane transport of Mg2+ will come from studies at subcellular levels, which aim at the isolation of transporters and their reconstitution. These studies should now be possible at least for Na/Mg exchange given our fair understanding of this system in intact red blood cells.
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