Hormone-sensitive magnesium transport in murine S49 lymphoma cells: characterization and specificity for magnesium

• Published in: The Journal of physiology 1983-04, Vol.337 (1), p.351-371
• Main Authors: Erdos, Joseph J., Maguire, Michael E.
• Format: Article
• Language: English
• Subjects: Animals; Biological Transport - drug effects; Calcium - metabolism; Calcium - pharmacology; Cells, Cultured; Hormones - pharmacology; Hot Temperature; Hydrogen-Ion Concentration; Isoproterenol - pharmacology; Lanthanum - pharmacology; Lymphoma - metabolism; Magnesium - metabolism; Manganese - metabolism; Mice; Neoplasms, Experimental - metabolism; Potassium Chloride - pharmacology; Scandium - pharmacology; Sodium Chloride - pharmacology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.1983.sp014628

1. The hormone-sensitive transport of Mg 2+ into murine S49 lymphoma cells and its relationship to other divalent cation transport systems have been investigated. 2. Mg 2+ influx, measured with 28 Mg 2+ , is saturable with an apparent extracellular ion concentration at half-maximal influx ( K in ) for Mg 2+ of 330 μM and a maximal influx rate of 360 p-mole/min.10 7 cells (2·9 n-mole/min.mg cell protein or a flux rate of about 0·12 p-mole/sec.cm 2 ). Efflux of Mg 2+ is biphasic with half-times of 55 and 240 min at 37 °C and is temperature-sensitive. 3. β-Adrenergic agonists inhibit influx but not efflux of Mg 2+ in S49 cells. Efflux of Mg 2+ is also unaffected by extracellular [Mg 2+ ] or [Ca 2+ ]. These results imply that the mechanism of the transport system does not involve Mg—Mg exchange. 4. Mn 2+ is a non-competitive inhibitor of Mg 2+ influx with an inhibition constant, K i , of about 200 μM. The weak inhibition exhibited by Ca 2+ ( K i > 5 mM) is also non-competitive. La 3+ inhibits Mg 2+ transport half-maximally at about 100 μM; Ni 2+ , Zn 2+ , Co 2+ and Sc 3+ are all less effective than La 3+ . The Ca 2+ -channel blockers cis -diltiazem, verapamil, and nifedipine and the monovalent cations Na + and K + also have no effect on Mg 2+ influx. However, increasing the extracellular pH stimulates Mg 2+ influx. 5. Total cellular Mg 2+ is about 85 n-mole/10 7 cells; however, at apparent isotopic equilibrium with 28 Mg 2+ less than 3% of total cellular Mg 2+ has been exchanged. This indicates that cellular Mg 2+ is highly compartmented and that recently transported Mg 2+ exchanges very slowly with bulk intracellular Mg 2+ . 6. Ca 2+ influx has a K in of 80 μM and is much slower than Mg 2+ influx. V max varied in different experiments from 3 to 15 p-mole/min.10 7 cells (25-125 p-mole/min.mg cell protein). Efflux of Ca 2+ is biphasic with half-times of 22 and 200 min and is temperature-sensitive. Hormonal stimulation has no effect on either influx or efflux of Ca 2+ . Mg 2+ is a competitive inhibitor of Ca 2+ influx ( K i = 3 mM). 7. Two kinetic components of Mn 2+ influx are present with apparent K in s of 4 μM and 100 μM. Maximal influx rates are 5 and 60 p-mole/min.10 7 cells (40 and 480 p-mole/min.mg cell protein), respectively. Influx of Mn 2+ is not altered by β-adrenergic agonist. 8. Uptake of Na + or K + is unaltered by β-adrenergic stimulation. These data in the S49 lymphoma cell indicate that (a) Mg 2+ is translocated by a transport sys