Previously, we have reported that ascorbic acid regulates calcium signaling in human larynx carcinoma HEp-2 cells. To evaluate the precise mechanism of Ca2+ release by ascorbic acid, the effects of specific inhibitors of the electron transport chain components on mitochondrial reactive oxygen species (ROS) production and Ca2+ mobilization in HEp-2 cells were investigated. It was revealed that the mitochondrial complex III inhibitor (antimycin A) amplifies ascorbate-induced Ca2+ release from intracellular stores. The mitochondrial complex I inhibitor (rotenone) decreases Ca2+ release from intracellular stores in HEp-2 cells caused by ascorbic acid and antimycin A. In the presence of rotenone, antimycin A stimulates ROS production by mitochondria. Ascorbate-induced Ca2+ release in HEp-2 cells is shown to be unaffected by catalase. The results obtained suggest that Ca2+ release in HEp-2 cells caused by ascorbic acid is associated with induced mitochondrial ROS production. The data obtained are in line with the concept of redox signaling that explains oxidant action by compartmentalization of ROS production and oxidant targets. 1. Introduction Redox processes involving transfer of electrons or hydrogen atoms are central processes of energy conversion in respiratory organisms. Recently, it has become apparent that numerous functionally significant biological processes proceed with participation of physical mechanisms ensuring intermolecular electron transfer. Electron transfer between low-molecular weight components of cytosol and intracellular proteins leads to the change of a functional state of both cellular proteins and cells as a whole [1, 2]. All biological systems contain redox elements that play an important role in transcriptional regulation, cell proliferation, apoptosis, hormonal signaling, and other fundamental cell functions [3]. Organization and coordination of the redox activity of these elements occur through redox circuits and depend on the intracellular concentration of redox-active molecules [4, 5]. Redox active molecules may cause both regulatory and toxic effects depending on the value of cellular redox state parameters [5, 6]. However, little is known about mechanisms of regulation, structural organization, and interaction between electron-transport participants inside the cell and other signal and regulatory systems. Recently new effects of such a redox-active molecule as ascorbic acid have been found. Beside numerous regulatory properties (hydroxylation of collagen, biosynthesis of carnitine and noradrenaline, etc.), selective
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