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Am J Physiol Cell Physiol (June 7, 2006). doi:10.1152/ajpcell.00217.2006
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Submitted on April 29, 2006
Accepted on June 1, 2006

MITOCHONDRIAL REACTIVE OXYGEN SPECIES AND Ca2+ SIGNALLING

Cristina Camello-Almaraz1, Pedro Julian Gomez-Pinilla1, Maria J. Pozo1, and Pedro Camello2*

1 Physiology, Univ of Extremadura, Caceres, Spain
2 Caceres, Spain; Physiology, Univ of Extremadura, Caceres, Spain

* To whom correspondence should be addressed. E-mail: pcamello{at}unex.es.

Mitochondria are an important source of reactive oxygen species formed as a side-product of oxidative phosphorylation. The main sites of oxidant production are complex I and complex III, where electrons flowing from reduced substrates are occasionally transferred to oxygen to form superoxide anion and derived products. These highly reactive compounds have a well known role in pathological states and in some cellular responses. However, though their link with Ca2+ is well studied in cell death, it has been hardly investigated in normal [Ca2+]i signals. Several Ca2+ transport systems are modulated by oxidation. Oxidation increases the activity of IP3 and ryanodine receptors, the main channels releasing Ca2+ from intracellular stores in response to cellular stimulation. On the other hand, mitochondria are known to control [Ca2+]i signals by Ca2+ uptake and release during cytosolic calcium mobilization, specially in mitochondria situated close to Ca2+ release channels. Mitochondrial inhibitors modify calcium signals in numerous cell types, including oscillations evoked by physiological stimulus. Although these inhibitors reduce mitochondrial Ca2+ uptake they also impair ROS production in several systems. In keeping with this effect, recent reports show that antioxidants or oxidant scavengers also inhibit physiological calcium signals. Furthermore, there is evidence that mitochondria generate ROS in response to cell stimulation, an effect suppressed by mitochondrial inhibitors which simultaneously block [Ca2+]i signals. Together, data reviewed here indicate that Ca2+ mobilizing stimulus generates mitochondrial ROS which, in turn, facilitate [Ca2+]i signals, a new aspect in the biology of mitochondria. Finally, the potential implications for biological modelling are discussed.




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