Abstract
The rapid mitochondrial uptake of calcium followed by slow release in certain pathophysiological states associated with an increase in intracellular calcium, to normalize the cytoplasmic levels of free calcium, provides an important protective mechanism against calcium cellular toxicity. Salicylic acid, an in vivo metabolite of aspirin, inhibits the uptake and enhances the release of calcium by mitochondria, thereby increasing the levels of cytoplasmic free calcium. The Ca2+ induced mitochondrial swelling is enhanced in the presence of salicylic acid and in which turn leads to loss of biosynthesis of ATP. These results suggest that salicylic acid may promote cellular damage in pathophysiological states associated with increase in intracellular free calcium.
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