Abstract
An increase in non-specific permeability across the plasma membrane of cells bathed in physiological media leads to an increase in intracellular Ca 2+. The extent of the increase depends on the extent of the membrane lesion; the duration of the increase depends on the metabolic capability of cells to pump Ca 2+ out. A slight, transient increase in cytosolic Ca 2+ can be beneficial because it activates repair mechanisms; a large, sustained, increase is toxic because it impairs normal cell function. Extracellular Ca 2+ prevents increases in non-specific permeability: only when the protective action of extracellular Ca 2+ is overcome by pore-forming agents does intracellular Ca 2+ rise to toxic levels. The beneficial actions of Ca 2+, superimposed on its damaging effect, account for some of the paradoxical effects of Ca 2+ that have been described in the literature.
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