Acute effect of EtOH on Mg21 homeostasis in liver cells: evidence for the activation of an Na1/Mg21 exchanger

Tessman, Patrick A., and Andrea Romani. Acute effect of EtOH on Mg21 homeostasis in liver cells: evidence for the activation of an Na1/Mg21 exchanger. Am. J. Physiol. 275 (Gastrointest. Liver Physiol. 38): G1106–G1116, 1998.—The acute administration of ethanol mobilizes a considerable amount of Mg21 from perfused rat livers and isolated hepatocytes in a dose-dependent fashion in the absence of release of cellular K1 or lactate dehydrogenase (LDH) in the extracellular medium. Mg21 extrusion becomes detectable within 2 min and reaches the maximum within 8 min after ethanol addition, declining toward the basal value thereafter irrespective of the persistence of alcohol in the perfusion system and the dose of ethanol administered. The effect is the result of a specific impairment of Mg21 transport and/or regulatory mechanisms. In fact, Mg21 extrusion does not occur under conditions in which 1) ethanol is replaced by an equivalent dose of DMSO, 2) amiloride or imipramine are used as inhibitors of the Na1/Mg21 exchanger, 3) extracellular Na1 is replaced by an equimolar concentration of choline chloride, and 4) 4-methylpyrazole is used to specifically inhibit alcohol dehydrogenase and cytochrome P-4502E1. Finally, the observation that the cellular level of ATP is markedly reduced after acute ethanol administration would suggest that Mg21 extrusion results from a decreased buffering capacity of cytosolic Mg-ATP complex.