Mitochondrial calcium transport and the redox nature of the calcium-induced membrane permeability transition.

Autor: Vercesi AE; Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, SP, Brazil. Electronic address: anibal@unicamp.br., Castilho RF; Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, SP, Brazil., Kowaltowski AJ; Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP, Brazil., de Oliveira HCF; Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas, SP, Brazil., de Souza-Pinto NC; Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP, Brazil., Figueira TR; Escola de Educação Física e Esporte de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil., Busanello ENB; Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, SP, Brazil.
Jazyk: angličtina
Zdroj: Free radical biology & medicine [Free Radic Biol Med] 2018 Dec; Vol. 129, pp. 1-24. Date of Electronic Publication: 2018 Aug 31.
DOI: 10.1016/j.freeradbiomed.2018.08.034
Abstrakt: Mitochondria possess a Ca 2+ transport system composed of separate Ca 2+ influx and efflux pathways. Intramitochondrial Ca 2+ concentrations regulate oxidative phosphorylation, required for cell function and survival, and mitochondrial redox balance, that participates in a myriad of signaling and damaging pathways. The interaction between Ca 2+ accumulation and redox imbalance regulates opening and closing of a highly regulated inner membrane pore, the membrane permeability transition pore (PTP). In this review, we discuss the regulation of the PTP by mitochondrial oxidants, reactive nitrogen species, and the interactions between these species and other PTP inducers. In addition, we discuss the involvement of mitochondrial redox imbalance and PTP in metabolic conditions such as atherogenesis, diabetes, obesity and in mtDNA stability.
(Copyright © 2018 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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