Defective translocation of PKCepsilon in EtOH-induced inhibition of Mg2+ accumulation in rat hepatocytes.

Background: Rats chronically fed ethanol for 3 weeks presented a marked decreased in total hepatic Mg(2+) content and required approximately 12 days to restore Mg(2+) homeostasis upon ethanol withdrawal. This study was aimed at investigating the mechanisms responsible for the EtOH-induced delay.

Methods: Hepatocytes from rats fed ethanol for 3 weeks (Lieber-De Carli diet-chronic model), rats re-fed a control diet for varying periods of time following ethanol withdrawal, and age-matched control rats fed a liquid or a pellet diet were used.

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

Liver cells from rats chronically fed a Lieber-De Carli diet for 3 wk presented a marked decreased in tissue Mg(2+) content and an inability to extrude Mg(2+) into the extracellular compartment upon stimulation with catecholamine, isoproterenol, or cell-permeant cAMP analogs. This defect in Mg(2+) extrusion was observed in both intact cells and purified liver plasma membrane vesicles. Inhibition of adrenergic or cAMP-mediated Mg(2+) extrusion was also observed in freshly isolated hepatocytes from control rats incubated acutely in vitro with varying doses of ethanol (EtOH) for 8 min.

Effect of thyroid hormone on Mg(2+) homeostasis and extrusion in cardiac cells.

The present study investigated the effect of alteration in thyroid hormone level on Mg(2+) homeostasis in cardiac ventricular myocytes. Hyperthyroid conditions increased cardiac myocytes total Mg(2+) content by ~14% as compared to cells from eu-thyroid animals. The excess Mg(2+) was localized predominantly within cytoplasm and mitochondria, and was mobilized into the extracellular compartment by addition of isoproterenol (ISO) or cAMP but not phenylephrine (PHE).

Involvement of ERK1/2 and p38 in Mg2+ accumulation in liver cells.

Activation of PKC signaling induces Mg(2+) accumulation in liver cells. To test the hypothesis that PKC induces Mg(2+) accumulation via MAPKs activation, hepatocytes were incubated in the presence of PD98059 and SB202190 as specific inhibitors of ERK1/2 and p38, respectively, and stimulated for Mg(2+) accumulation by addition of PMA or OAG. Accumulation of Mg(2+) within the cells was measured by atomic absorbance spectrophotometry in the acid extract of cell pellet.

Role of glucose in modulating Mg2+ homeostasis in liver cells from starved rats.

Alpha1- and beta-adrenoceptor stimulation elicits Mg2+ extrusion from liver cells in conjunction with hepatic glucose output (T. Fagan and A. Romani.