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LIVER AND BILIARY TRACT

Delayed restoration of Mg²⁺ content and transport in liver cells following ethanol withdrawal

¹Department of Physiology and Biophysics, and ²Division of Pathology, Case Western Reserve University, Cleveland, Ohio

Submitted November 14, 2008 ; accepted in final form June 23, 2009

Liver cells from rats chronically fed a Lieber-De Carli diet for 3 wk presented a marked decreased in tissue Mg²⁺ content and an inability to extrude Mg²⁺ into the extracellular compartment upon stimulation with catecholamine, isoproterenol, or cell-permeant cAMP analogs. This defect in Mg²⁺ extrusion was observed in both intact cells and purified liver plasma membrane vesicles. Inhibition of adrenergic or cAMP-mediated Mg²⁺ extrusion was also observed in freshly isolated hepatocytes from control rats incubated acutely in vitro with varying doses of ethanol (EtOH) for 8 min. In this model, however, the defect in Mg²⁺ extrusion was observed in intact cells but not in plasma membrane vesicles. In the chronic model, upon removal of EtOH from the diet hepatic Mg²⁺ content and extrusion required 10 days to return to normal level both in isolated cells and plasma membrane vesicles. In hepatocytes acutely treated with EtOH for 8 min, more than 60 min were necessary for Mg²⁺ content and extrusion to recover and return to the level observed in EtOH-untreated cells. Taken together, these data suggest that in the acute model the defect in Mg²⁺ extrusion is the result of a limited refilling of the cellular compartment(s) from which Mg²⁺ is mobilized upon adrenergic stimulation rather than a mere defect in adrenergic cellular signaling. The chronic EtOH model, instead, presents a transient but selective defect of the Mg²⁺ extrusion mechanisms in addition to the limited refilling of the cellular compartments.

Mg²⁺ homeostasis; hepatocyte; catecholamine; plasma membrane