Characterization of magnesium efflux from Ehrlich ascites tumor cells

Magnesium efflux from intact Ehrlich ascites tumor cells (EATC) has been characterized under 0-trans conditions. It is shown that a magnesium-extruding mechanism operates in these cells which brings about magnesium efflux up to 20% of the cell total content. EATC magnesium efflux is independent from extracellular Ca2+ and its apparent velocity is not affected by [Mg2+]o up to 160 microM. This extrusion, however, is strictly dependent on extracellular Na+ and it is inhibited by ouabain (1 mM), amiloride (1 mM), imipramine (0.5 mM) and quinidine (1 mM). It is not affected by HMA (5-N,N-hexamethylene) amiloride) (0.5 microM) and vanadate (0.1 mM). Bumetanide (0.5 mM) enhances magnesium extrusion in these cells. EATC magnesium extrusion can be significantly stimulated by db cAMP, forskolin, and IBX (3-isobutyl-1-methyl-xanthine). The intracellular magnesium distribution, studied also by means of the ionophore A23187, is regulated by energy metabolism and cell ATP content. Altogether our data demonstrate that EATC exhibit a magnesium extrusion sustained by Na+ gradient across the plasma membrane and carried out by a Na+/Mg2+ antiport. In these cells magnesium homoeostasis results, regulated efficiently by cell ATP and cAMP content.