Regular ArticleThe Participation of Reactive Oxygen Species and Protein Thiols in the Mechanism of Mitochondrial Inner Membrane Permeabilization by Calcium plus Prooxidants
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Mitochondrial bioenergetics and redox dysfunctions in hypercholesterolemia and atherosclerosis
2020, Molecular Aspects of MedicineCitation Excerpt :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. This strongly supports the notion that H2O2 participates in this process due to its ability to promote protein dithiol formation (Fagian et al., 1990; Kowaltowski et al., 2001).
Mitochondrial calcium transport and the redox nature of the calcium-induced membrane permeability transition
2018, Free Radical Biology and MedicineCitation Excerpt :Further work [270–272] supports these findings as well as a role for the p53-CypD complex in the mechanisms of PTP-induced cell death. The evidence that MPT induced by Ca2+ was stimulated by thiol oxidation [203,216,256,257] and by exogenous oxidant generating systems such as xanthine/xanthine oxidase [273,274], menadione [275], nitrofurantoin [276] and 5-aminolevulinic acid [257,277] and depletion of mitochondrial NADPH [178,259] and, in contrast, protected by a variety of antioxidants [256,258,278–281] or the absence of molecular oxygen [263] led the Vercesi group to directly test the hypothesis that MPT was caused by mitochondrially-generated oxidants. Indeed, strong evidence for the participation of H2O2 was obtained in studies demonstrating protection against MPT by catalase [174,256,263,278,282], peroxiredoxin [279] and o-phenanthroline [263].
Omega-3 polyunsaturated fatty acids and mitochondria, back to the future
2017, Trends in Food Science and TechnologyCyclophilin D deficiency rescues Aβ-impaired PKA/CREB signaling and alleviates synaptic degeneration
2014, Biochimica et Biophysica Acta - Molecular Basis of DiseaseProtective action of tamoxifen on carboxyatractyloside-induced mitochondrial permeability transition
2011, Life SciencesCitation Excerpt :This work describes the results of experiments aimed at placing on a firmer ground the knowledge about the mechanism by which tamoxifen inhibits mitochondrial permeability transition. It has been documented that the opening of the non-specific pore may occur following an oxidative stress (Valle et al., 1993; Halestrap et al., 1997; Kushnareva and Sokolove, 2000; García et al., 2009b). Thus, those reagents that might neutralize oxidant radicals should be effective inhibitors of membrane leakage, and tamoxifen appears to meet this condition.