Ascorbic acid is an endogenous cytosolic inhibitor of ATP-supported rat liver mitochondrial calcium transport.
ATP-supported but not Site I or Site II respiratory chain-linked 45Ca2+ transport into isolated rat liver mitochondria is profoundly inhibited by a small molecule present in the cytosolic fraction. This inhibitor was purified and shown to be identical with ascorbic acid in a number of chemical properties, cytosolic abundance, susceptibility to ascorbate oxidase, and to agents that otherwise block the effect of authentic ascorbic acid. Experiments with a variety of free radical scavengers and glutathione indicated that ascorbate inhibition of calcium transport is mediated through a 1-electron-free radical mechanism rather than a conventional 2-electron reaction. Calcium transport mechanisms may, therefore, be a target in the pathophysiology of disease processes that influence the intracellular ratios and levels of ascorbate and physiological radical scavengers.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D005609:Free Radicals; D005978:Glutathione / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D005609:Free Radicals; D000255:Adenosine Triphosphate; D005978:Glutathione; D001205:Ascorbic Acid; D002118:Calcium