ArticleAlcoholism, clinical and experimental research2013
Acute effect of ethanol on hepatic reticular G6Pase and Ca2+ pool.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHydrolysis of glucose 6-phosphate (G6P) via glucose 6-phosphatase (G6Pase) enlarges the reticular Ca(2+) pool of the hepatocyte. Exposure of liver cells to ethanol (EtOH) impairs reticular Ca(2+) homeostasis. The present study investigated the effect of acute EtOH administration on G6P-supported Ca(2+) accumulation in liver cells.
methodsTotal microsomes were isolated from rat livers acutely perfused with varying doses of EtOH (0.01, 0.1, or 1% v/v) for 8 minutes. Calcium uptake was assessed by (45) Ca redistribution. Inorganic phosphate (Pi) formation was measured as an indicator of G6Pase hydrolytic activity.
resultsG6P-supported Ca(2+) uptake decreased in a manner directly proportional to the dose of EtOH infused in the liver, whereas Ca(2+) uptake via SERCA pumps was decreased by ~25% only at the highest dose of alcohol administered. The reduced accumulation of Ca(2+) within the microsomes resulted in a smaller inositol 1,4,5-trisphosphate (IP(3))-induced Ca(2+) release. Kinetic assessment of IP(3) and passive Ca(2+) release indicated a faster mobilization in microsomes from EtOH-treated livers, suggesting alcohol-induced alteration of Ca(2+) releasing mechanisms. Pretreatment of livers with chloromethiazole (CMZ) or dithiothreitol (DTT), but not 4-methyl-pyrazole prevented the inhibitory effect of EtOH on G6Pase activity and Ca(2+) homeostasis.
conclusionsLiver G6Pase activity and IP(3) -mediated Ca(2+) release are rapidly inhibited following acute (8 minutes) exposure to EtOH, thus compromising the ability of the endoplasmic reticulum to dynamically modulate Ca(2+) homeostasis in the hepatocyte. The protective effect of CMZ and DTT suggests that the inhibitory effect of EtOH is mediated through its metabolism via reticular cyP4502E1 and consequent free radicals formation.
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