Abstract
Induction of mitochondrial swelling and increased generation of reactive oxygen forms by Ca ions have been shown in suspension of mitochondria from rat uterus. These effects were suppressed by the blocker of mitochondrial Ca2+-uniporter ruthenium red and MPTP inhibitor cyclosporin A, that evidences that the induction of mitochondrial permeability transition pore by Ca ions takes place. Ca2+-induced mitochondrial swelling was blocked by ATP-sensitive channel blocker glybenclamide but only if K+ was present in the incubation medium. We also demonstrated that Ca2+-induced mitochondrial swelling can be eliminated in the presence of ROS scavengers N-acetyl cysteine and ascorbate. This effect of scavengers was also sensitive to K+ and was not revealed in the medium that contained equimolar NaCl instead of KCl. Thus, our data gave us grounds to assume that the induction of MPTP by Ca ions evokes the activation of mitochondrial ATPsensitive K+-channels, which are mediated by ROS.
Highlights
We have previously demonstrated activation of ATP- and diazoxide-sensitive K-trasporter in mitochondria of rat uterine smooth muscle by photoncorrelation spectroscopy and detection of side scattering in suspension of myometrium mitochondria. [12, 13]
Registrations of side scattering correlate with data of measurement of hydrodynamic diameter (HD) of mitochondria obtained using the method of photon-correlation spectroscopy of isolated mitochondria of the rat myometrium [13]
Addition of 100 μМ СаCl2 resulted in a faster swelling rate and in higher steady-state volume (Fig. 1, curves 2). This effect of Ca ions was reversed by known blocker of Ca2+-uniporter in mitochondria ruthenium red (RuR) (10 μМ) as well as by the blocker of the mitochondria permeability transition pore (MPTP) cyclosporine A (10 μМ)
Summary
We have previously demonstrated activation of ATP- and diazoxide-sensitive K-trasporter in mitochondria of rat uterine smooth muscle by photoncorrelation spectroscopy and detection of side scattering in suspension of myometrium mitochondria. [12, 13]. We have previously demonstrated activation of ATP- and diazoxide-sensitive K-trasporter in mitochondria of rat uterine smooth muscle by photoncorrelation spectroscopy and detection of side scattering in suspension of myometrium mitochondria. The evidence has been presented of the sensitivity of accumulation of Са ions in mitochondria to presence of activators of mitoKАТР [8, 11] It has been demonstrated [8, 11] that activation of the channel may regulate Ca2+ transport into mitochondrial matrix without damage to the vital capacity of organelle itself. According to these results, mitoKАТР may be an additional factor in the regulation of homeostasis of Ca2+ in a cell. The aim of the work was to study the effect of Са2+ in high concentrations on glybenclamidesensitive transport of K+ in mitochondria of smooth muscle of the uterus
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