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10.1016/j.metabol.2010.03.019

http://scihub22266oqcxt.onion/10.1016/j.metabol.2010.03.019
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20494376!2928872!20494376
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suck abstract from ncbi


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pmid20494376      Metabolism 2010 ; 59 (11): 1663-71
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  • Adenosine triphosphate depletion by cyanide results in a Na(+)-dependent Mg(2+) extrusion from liver cells #MMPMID20494376
  • Dalal P; Romani A
  • Metabolism 2010[Nov]; 59 (11): 1663-71 PMID20494376show ga
  • Addition of NaCN to isolated hepatocytes results in a marked and rapid decrease in cellular adenosine triphosphate (ATP) content, and in the extrusion of a sizable amount of cellular Mg(2+). This extrusion starts after a 10-minute lag phase and reaches a maximum of 35 to 40 nmol Mg(2+) per milligram protein within 60 minutes from the addition of CN(-). A quantitatively similar Mg(2+) extrusion is also observed after the addition of the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenylhydrazone but not that of the glycolysis inhibitor iodoacetate. The Mg(2+) extrusion is completely inhibited by the removal of extracellular Na(+) or the addition of imipramine, quinidine, or glibenclamide, whereas it persists after the removal of extracellular Ca(2+) or K(+), or the addition of amiloride. An acidic extracellular pH or the removal of extracellular HCO(3)(-) inhibits the cyanide-induced Mg(2+) extrusion by at least 80%. Taken together, these data suggest that the decrease in cellular adenosine triphosphate content removes a major Mg(2+) complexing agent from the hepatocyte and results in an extrusion of hepatic Mg(2+) exclusively through a Na(+)-dependent exchange mechanism modulated by acidic changes in extracellular pH.
  • |Adenosine Triphosphate/*deficiency[MESH]
  • |Animals[MESH]
  • |Cells, Cultured[MESH]
  • |Cyanides/*pharmacology[MESH]
  • |Hepatocytes/*metabolism[MESH]
  • |Hydrogen-Ion Concentration[MESH]
  • |Magnesium/*metabolism[MESH]
  • |Male[MESH]
  • |Rats[MESH]
  • |Rats, Sprague-Dawley[MESH]


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