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Effect of Repeated Doses of Ethanol on Hepatic Mg 2+ Homeostasis and Mobilization
Author(s) -
Young Andrew,
BertiMattera Liliana,
Romani Andrea
Publication year - 2007
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2007.00408.x
Subject(s) - agonist , endoplasmic reticulum , chemistry , endocrinology , medicine , stimulation , homeostasis , cytosol , ethanol , adrenergic agonist , adrenergic , cytoplasm , receptor , biochemistry , biology , enzyme
The acute administration of a first dose of ethanol (EtOH) to rat liver cells reduces the amount of Mg 2+ extruded by a second dose of EtOH or the subsequent addition of adrenergic agonists. In contrast, the Mg 2+ extrusion normally elicited by the α 1 ‐adrenergic or β ‐adrenergic agonist does not impair the Mg 2+ mobilization induced by the subsequent addition of EtOH. Inhibition of EtOH metabolism by 4‐methylpyrazole abolishes almost completely the Mg 2+ extrusion induced by the first dose of EtOH, and partially enlarges that elicited by the second dose of alcohol or the subsequent adrenergic stimulation. Ethanol‐treated liver cells stimulated by the adrenergic agonist show a reduced level of membrane‐bound G α s as well as a reduced cellular cAMP content. Analysis of cellular Mg 2+ distribution indicates that EtOH administration decreases the Mg 2+ content of the cytoplasm, mitochondria, and endoplasmic reticulum to a comparable extent. These data indicate that acute EtOH administration directly impairs cellular Mg 2+ homeostasis and also prevents a further Mg 2+ mobilization by additional doses of alcohol or α 1 ‐adrenoceptor and β ‐adrenoceptor agonist by decreasing cytosolic and intraorganelle Mg 2+ content and by affecting G‐protein membrane distribution/signaling.