title: Mechanisms, regulation and pathologic significance of Mg2+ efflux from erythrocytes.
abstract: Mg2+ efflux from erythrocytes can be performed by the Na+/Mg2+ antiport and by Na+-independent Mg2+ efflux. Na+-independent Mg2+ efflux functions via the unspecific choline exchanger as choline/Mg2+ or K+/Mg2+ antiport and as Mg2+ efflux accompanied by intracellular Cl- for charge compensation, as found for example in sucrose medium. Na+/Mg2+ antiport in erythrocytes exchanges 2 extracellular Na+ for 1 intracellular Mg2+. Driving forces are the Na+ and Mg2+ gradients. By reversing these gradients, the Na+/Mg2+ antiporter can mediate Mg2+ influx. The Na+/Mg2+ antiporter can exchange 24Mg2+ for 28Mg2+ and other divalent cations for intracellular Mg2+. In the exchange mechanism, extra- and intracellular Na+ can compete with Mg2+. Na+/Mg2+ antiport is inhibited by amiloride, quinidine and imipramine. Na+/Mg2+ antiport is drastically activated by intracellular Mg2+ due to an allosteric transition. The affinity of intracellular Mg2+ to the Na+/Mg2+ antiporter is dependent on intracellular ATP due to phosphorylation. Besides this mechanism, in non Mg2+-loaded erythrocytes, the activity of Na+/Mg2+ antiport is regulated by phosphorylation-dephosphorylation and by intracellular Cl-. The drastically Mg2+-activated Na+/Mg2+ antiporter is not further stimulated by phosphorylation and intracellular Cl-. Na+-independent Mg2+ efflux via the choline exchanger is also inhibited by amiloride, quinidine and imipramine, and can also be regulated by phosphorylation-dephosphorylation. Na+/Mg2+ antiport of erythrocytes is altered in various pathologic conditions.
authors.affiliation: Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Institut für Molekularbiologie und Biochemie, Arnimallee 22, 14195 Berlin, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Günther
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology; D000755:Anemia, Sickle Cell / Q000503:physiopathology; D000818:Animals; D017920:Antiporters / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology; D002794:Choline / Q000378:metabolism; D003550:Cystic Fibrosis / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000503:physiopathology; D004912:Erythrocytes / Q000378:metabolism*; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D008274:Magnesium / Q000097:blood*; D008275:Magnesium Deficiency / Q000503:physiopathology; D019964:Mood Disorders / Q000503:physiopathology; D010766:Phosphorylation; D012964:Sodium / Q000502:physiology; D013395:Sucrose / Q000494:pharmacology
chemical_list: D017920:Antiporters; D002712:Chlorides; D005609:Free Radicals; C046250:sodium-magnesium antiporter; D013395:Sucrose; D000255:Adenosine Triphosphate; D012964:Sodium; D008274:Magnesium; D002794:Choline