Calcium and mitochondria

The literature suggests that the physiological functions for which mithochondria sequester Ca2+ are (1) to stimulate and control the rate of oxidative phosphorylation, (2) to induce the mithochondrial permeability transition (MPT) and perhaps apoptotic cell death, and (3) to modify the shape of cytosolic Ca2+ pulses or transients. There is strond evidence that intramithochondrial Ca2+ controls both the rate of ATP production by oxidative phosphorylation and induction of the MPT. Since the results of these processes are so divergent, the signals inducing them must not be ambiguous. Futhermore, as pointed out by Balaban [J. Mol. Cel. Cardiol. 34 (2002) 11259-11271]. for any repetitive physiological process dependant on intramitochondrial free Ca2+ concentation ([Ca2+](m)), a kind of intramithochondrial homestatis must exist so that Ca2+ influx durung the pulse is matched Ca2+ efflux during the period between pulses to avoid either Ca2+ buildup or depletion. In addition, mithochondrial Ca2+ transport modifies both spatial and temporal aspects of cytosolic Ca2+ signaling. Here, we look at the amounts of Ca2+ necessary to mediate the functions of mithochondrial Ca2+ transport and at the mechanisms of transport themselves in order to set up a hypothesis about how the mechanisms carry out their roles. the emphasis here is on isolated mithochondria and on general mithochondria properties in order to focus on how mithochondria alone may function to fulfill their physiological roles even though the interactions of mithochondria with other organelles, particularly with endoplasmic and sacroplasmic reticulum [Sci. STKE re1 (2204) 1-p], may also infuence this story. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All right reserved.