Background & Objective: Permeability transition pore (PTP) is central for apoptosis by acting as a good candidate pathway for the release of cytochrome c and apoptosis-induction factors from mitochondria. Arsenite may induce apoptosis via a direct effect on PTP. To characterize the exact mechanism for arsenite to induce PTP opening, the correlations of calcium-induced calcium release from mitochondria (mCICR) to As2O3-induced PTP opening and cytochrome c release from mitochondria were studied.
Methods: Mitochondria were prepared from Wistar rat livers. The effect of As2O3 on mitochondrial PTP opening was measured with ultraviolet (UV) spectrophotometer. The changes of Ca(2+) concentration were detected with UV spectrophotometer to monitor Ca(2+) -induced Ca(2+) release from mitochondria. Cytochrome c release mediated by Ca(2+) was measured with Western blot.
Results: As2O3 (10 micromol/L) combined with low concentration of Ca(2+) didn't induce PTP opening and cytochrome c release from mitochondria; while As2O3 (10 micromol/L) combined with high concentration of Ca(2+) induced PTP opening and cytochrome c release. When mCICR was inhibited, the effect of As2O3 and Ca(2+) on PTP opening and cytochrome c release was completely inhibited.
Conclusion: As2O3-induced PTP opening and cytochrome c release depend on mCICR.
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Programmed cell death (apoptosis) is essential part of the process of tissue regeneration that also plays role in the mechanism of pathology. The phenomenon of fast and transient permeability of mitochondrial membranes by various triggers, known as permeability transition pore (mPTP) leads to the release of proapoptotic proteins and acts as an initial step in initiation of apoptosis. However, a role for mPTP was also suggested for physiology and it is unclear if there is a threshold in number of mitochondria with mPTP which induces cell death and how this mechanism is regulated in different tissues.
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