Stimulation of Na + /Mg 2+ antiport in rat erythrocytes by intracellular Cl −

Archives of Biochemistry and Biophysics

2011

436

425

Magnesium, the second most abundant cellular cation after potassium, is essential to regulate numerous cellular functions and enzymes, including ion channels, metabolic cycles, and signaling pathways, as attested by more than 1000 entries in the literature. Despite significant recent progress, however, our understanding of how cells regulate Mg2+ homeostasis and transport still remains incomplete. For example, the occurrence of major fluxes of Mg2+ in either direction across the plasma membrane of mammalian cells following metabolic or hormonal stimuli has been extensively documented. Yet, the mechanisms ultimately responsible for magnesium extrusion across the cell membrane have not been cloned. Even less is known about the regulation in cellular organelles. The present review is aimed at providing the reader with a comprehensive and up-to-date understanding of the mechanisms enacted by eukaryotic cells to regulate cellular Mg2+ homeostasis and how these mechanisms are altered under specific pathological conditions.

Section: Mg2+ Transport Mechanismssupporting

confidence: 71%

Section: Mg2+ Transport Mechanismssupporting

confidence: 65%

Section: Mg2+ Transport Mechanismsmentioning

confidence: 85%

See 1 more Smart Citation

Cellular magnesium homeostasis

Archives of Biochemistry and Biophysics

2011

436

425

Magnesium Homeostasis in Mammalian Cells

Metal Ions in Life Sciences

2012

Magnesium, the second most abundant cation within the cell, plays an important role in numerous biological functions. Experimental evidence indicates that mammalian cells tightly regulate cellular magnesium ion content through specific mechanisms controlling Mg(2+) entry and efflux across the cell membrane and the membrane of various cellular organelles as well as intracellular Mg(2+) buffering under resting conditions and following hormonal and metabolic stimuli. This chapter will provide an assessment of the various mechanisms controlling cellular Mg(2+) homeostasis and transport, and the implications changes in cellular Mg(2+) content play under physiological and pathological conditions.

Modulation of Na+/Mg2+ exchanger stoichiometry ratio by Cl− ions in basolateral rat liver plasma membrane vesicles

Cefaratti

2011

Mol Cell Biochem

The Na+/Mg²+ exchanger represents the main Mg²+ extrusion mechanism operating in mammalian cells including hepatocytes. We have previously reported that this exchanger, located in the basolateral domain of the hepatocyte, promotes the extrusion of intravesicular trapped Mg²+ for extravesicular Na+ with ratio 1. This electrogenic exchange is supported by the accumulation of tetraphenyl-phosphonium within the vesicles at the time when Mg²+ efflux occurs. In this present study, the role of extra- and intra-vesicular Cl⁻ on the Na+/Mg²+ exchange ratio was investigated. The results reported here suggest that Cl⁻ ions are not required for the Na+ to Mg²+ exchange to occur, but the stoichiometry ratio of the exchanger switches from electrogenic (1Na(in)+ :1Mg(out)²+) in the presence of intravesicular Cl⁻ to electroneutral (2Na(in)+ :1 Mg(out)²+) in their absence. In basolateral liver plasma membrane vesicles loaded with MgCl₂ labeled with ³⁶Cl⁻, a small but significant Cl⁻ efflux (~30 nmol Cl⁻/mg protein/1 min) is observed following addition of NaCl or Na-isethionate to the extravesicular medium. Both Cl⁻ and Mg²+ effluxes are inhibited by imipramine but not by amiloride, DIDS, niflumic acid, bumetanide, or furosemide. In vesicles loaded with Mg-gluconate and stimulated by Na-isethionate, an electroneutral Mg²+ extrusion is observed. Taken together, these results suggest that the Na+/Mg²+ exchanger can operate irrespective of the absence or the presence of Cl⁻ in the extracellular or intracellular environment. Changes in trans-cellular Cl⁻ content, however, can affect the modus operandi of the Na+/Mg²+ exchanger, and consequently impact "cellular" Na+ and Mg²+ homeostasis as well as the hepatocyte membrane potential.