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The interaction of mitochondria with pulses of calcium

Mitochondria seem to be distributed within cells so as to provide the necessary amounts of ATP when and where it is needed. In muscle tissue many mitochondria are located near the contracting filaments. In cells which make and secrete large amounts of protein many mitochondria are found near the rough endoplasmic reticulum. In neurons mitochondria use energy to move in an anterograde direction through the axon on microtubules and later return in the retrograde direction, distributing themselves, in the process, along the axon. In all cells there are a significant number of mitochondria near the nucleus. For years, we have known of the mitochondrial calcium uniporter, of the Na+-dependent and Na+independent efflux mechanisms, and of the permeability transition pore [2]. More recently, work first with aequorin and then with artificially synthesized fluorescent calcium indicators showed that the levels of calcium within the cytosol of cells are low – in the range of 100 nM, except during calcium transients or pulses that often pass like waves through the cytosol [1]. The calcium within these pulses or transients comes, in large part, from release from intracellular stores, replenished by calcium influx from the extracellular space through calcium channels. These intracellular stores are found in the sarcoplasmic reticulum of muscle tissue and generally within the endoplasmic reticulum of other tissue. During these calcium pulses or transients the cytosolic calcium concentration ([Ca2+]) rises into the range from 0.5 to over 1.0 μM. In restricted regions near the pores effluxing calcium from intracellular stores, the [Ca2+] can go even higher. Several reactions within the intramitochondrial metabolic pathways have been found to be activated by calcium[1]. Of these, those catalyzed by three dehydrogenases coupled to the TCA cycle (pyruvate dehydrogenase, alpha keto gluterate dehydrogenase, and isocitrate dehydrogenase) are the best known; however, the electron transport system within liver mitochondria, the F1 ATPase, and the adenine nucleotide translocase have also been found to be stimulated by calcium. The advocates of metabolic control theory support the view that there is not a single rate-limiting step for the intramitochondrial metabolic reactions and that calcium acts to coordinate the activation of several steps among which rate limitation is shared so as to increase the rate of ATP production (for review, see [1]). The kinetics of the influx and efflux of calcium through the uniporter and the Na+-dependent and Na+independent efflux mechanisms are known for the most frequently studied types of mitochondria (liver and heart) [2]. Calculations of the amount of calcium taken up by mitochondria from calcium pulses like those observed in cells originally led to the conclusion that this calcium uptake would be insufficient to activate the intramitochondrial calcium-dependent metabolic reactions, except in those cases where the mitochondria are located near the intracellular stores from which the calcium in the calcium pulses is