Calcium and ischemic brain damage.
An account is given of calcium metabolism in the brain, with particular reference to the possibility that loss of calcium homeostasis is the cause of ischemic neuronal necrosis. The hypothesis of calcium-related cell damage is based on the fact that dense ischemia leads to an influx of calcium into cells, and that raised intracellular calcium concentrations activate lipases and proteases, and cause disaggregation of neurotubuli and enhanced protein phosphorylation. Such changes have the potential of inducing membrane damage and dysfunction of intracellular transport mechanisms. An attempt is made to critically review available evidence on the calcium hypothesis of cell death.
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002118:Calcium / Q000378:metabolism*; D002463:Cell Membrane Permeability; D006801:Humans; D008049:Lipase / Q000378:metabolism; D009336:Necrosis; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D051381:Rats
D009419:Nerve Tissue Proteins; D008049:Lipase; D010447:Peptide Hydrolases; D002118:Calcium