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Am J Physiol Gastrointest Liver Physiol 284: G57-G67, 2003; doi:10.1152/ajpgi.00153.2002
0193-1857/03 $5.00
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Vol. 284, Issue 1, G57-G67, January 2003

Chronic EtOH administration alters liver Mg2+ homeostasis

Andrew Young, Christie Cefaratti, and Andrea Romani

Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4970

Ethanol (EtOH) administration to rats for 4 wk markedly decreased Mg2+ content in several tissues, including liver. Total cellular Mg2+ accounted for 26.8 ± 2.4 vs. 36.0 ± 1.4 nmol Mg2+/mg protein in hepatocytes from EtOH-fed and control rats, respectively, and paralleled a 13% decrease in cellular ATP content. Stimulation of alpha 1- or beta -adrenergic receptor or acute EtOH administration did not elicit an extrusion of Mg2+ from liver cells of EtOH-fed rats while releasing 5% of total tissue Mg2+ content from hepatocytes of control rats. Despite the 25% decrease in Mg2+ content, hepatocytes from EtOH-fed rats did not accumulate Mg2+ following stimulation of protein kinase C signaling pathway, whereas control hepatocytes accumulated ~2 nmol Mg2+ · mg protein-1 · 4 min-1. Together, these data indicate that Mg2+ homeostasis and transport are markedly impaired in liver cells after prolonged exposure to alcohol. The inability of liver cells, and possibly other tissues, to accumulate Mg2+ can help explain the reduction in tissue Mg2+ content following chronic alcohol consumption.

hepatocytes; protein kinase C; adrenergic signaling; plasma membranes


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