Removal of calcium overload caused by A23187 is more dependent on glycolysis than oxidative phosphorylation.
An increase of cytosol Ca2+ may be the mediator of irreversible cell damage after ATP depletion. Ca2+ influx can also be induced by addition of the ionophore A23187. The extent of cell damage caused by A23187 during concomitant metabolic inhibition was investigated on quiescent fibroblasts. Inhibition of glycolysis resulted in increased cell damage compared to control, whereas an increased rate of glycolysis during inhibition of oxidative phosphorylation attenuated cell damage. These results indicate that glycolysis plays an important part in the removal of entering Ca2+.
Department of Clinical Chemistry, Odense University Hospital, Denmark.
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Kristensen
D000255:Adenosine Triphosphate / Q000378:metabolism; D000968:Antimycin A; D000001:Calcimycin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line / Q000187:drug effects; D005947:Glucose; D006019:Glycolysis / Q000187:drug effects; D006801:Humans; D007460:Iodoacetamide; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D010085:Oxidative Phosphorylation; D013997:Time Factors
D000001:Calcimycin; D000968:Antimycin A; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D005947:Glucose; D002118:Calcium; D007460:Iodoacetamide