Original contributionPermeabilization of the inner mitochondrial membrane by Ca2+ ions is stimulated by t-butyl hydroperoxide and mediated by reactive oxygen species generated by mitochondria
References (29)
- et al.
Role of Ca2+ in toxic cell killing
Trends Pharmacol. Sci.
(1989) - et al.
Mechanism of calcium potentiation of oxygen free radical injury to renal mitochondria
J. Biol. Chem.
(1986) - et al.
Generation of reactive oxygen metabolites and oxidative damage in mitochondria: The role of calcium
- et al.
Stoichiometry of H+ ejection and Ca2+ uptake coupled to electron transport in rat heart mitochondria
J. Biol. Chem.
(1978) - et al.
Membrane protein thiol cross-linking associated with the permeabilization of the inner mitochondrial membrane by Ca2+ plus prooxidants
J. Biol. Chem.
(1990) - et al.
The participation of reactive oxygen species and protein thiols in the mechanism of mitochondrial membrane permeabilization by Ca2+ plus prooxidants
Arch. Biochem. Biophys.
(1993) - et al.
The giant channel of the inner mitochondrial membrane is inhibited by cyclosporin A
J. Biol. Chem.
(1991) - et al.
Modulation of the mitochondrial permeability transition pore
J. Biol. Chem.
(1992) - et al.
Modulation of the mitochondrial megachannel by divalent cations and protons
J. Biol. Chem.
(1992) Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore by the proton electrochemical gradient
J. Biol. Chem.
(1992)
t-Butyl hydroperoxide-induced radical production in rat liver mitochondria
Free Radic. Biol. Med.
Method of determining oxygen concentrations in biological media, suitable for calibration of the electrode
Anal. Biochem.
Considerations in the spin trapping of superoxide and hydroxyl radical in aqueous systems using 5,5-dimethyl-l-pyrroline-l-oxide
Biochem. Biophys. Res. Commun.
The catalase requirement in the reversal of mitochondrial swelling caused by reduced glutathione and by trace metals
J. Biol. Chem.
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2020, Molecular Aspects of MedicineCitation Excerpt :The evidence that cyclosporin A (CsA), a pore-opening inhibitor (Crompton et al., 1988; Broekemeier et al., 1989), prevents cell death under different pathological conditions (Griffiths and Halestrap, 1993; Bernardi et al., 2006) supports the participation of this pore in the pathogenesis of ischaemia/reperfusion, heart and neurodegenerative diseases, traumatic brain injury, muscular dystrophy, inflammation, dyslipidaemias, drug toxicity and ageing (Griffiths and Halestrap, 1993; Bernardi et al., 2006; Halestrap and Pasdois, 2009; Vaseva et al., 2012). The redox hypothesis for mPTP regulation is further supported by the protection against it opening by several antioxidants (Vercesi et al., 2018) or the absence of molecular oxygen (Castilho et al., 1995a). In addition, evidence has shown that exogenous catalase (Valle et al., 1993; Castilho et al., 1995a; Kowaltowski et al., 1996), peroxiredoxin (Kowaltowski et al., 1998) or o-phenanthroline (Castilho et al., 1995a) prevents opening of the mPTP.
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