Calorie restriction decreases endogenous H2O2 generation per O2 consumed and increases viability in S. cerevisiae (2004)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Subjects: SACCHAROMYCES; BIOQUÍMICA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Programa e Resumos
- Conference titles: Reunião Anual da Sociedade Brasileira de Bioquímica e Biologia Molecular
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ABNT
BARROS, Mário Henrique de et al. Calorie restriction decreases endogenous H2O2 generation per O2 consumed and increases viability in S. cerevisiae. 2004, Anais.. São Paulo: SBBq, 2004. . Acesso em: 19 abr. 2024. -
APA
Barros, M. H. de, Bandy, B., Tahara, E. B., & Kowaltowski, A. J. (2004). Calorie restriction decreases endogenous H2O2 generation per O2 consumed and increases viability in S. cerevisiae. In Programa e Resumos. São Paulo: SBBq. -
NLM
Barros MH de, Bandy B, Tahara EB, Kowaltowski AJ. Calorie restriction decreases endogenous H2O2 generation per O2 consumed and increases viability in S. cerevisiae. Programa e Resumos. 2004 ;[citado 2024 abr. 19 ] -
Vancouver
Barros MH de, Bandy B, Tahara EB, Kowaltowski AJ. Calorie restriction decreases endogenous H2O2 generation per O2 consumed and increases viability in S. cerevisiae. Programa e Resumos. 2004 ;[citado 2024 abr. 19 ] - Caloric restriction protects mice against isoproterenol-induced cardiac hypertrophy by mechanisms that involve mitochondrial ATP sensitive potassium channel and modulation of redox state
- Bioenergetic consequences of opening the ATP-sensitive `K POT. +´ channel of heart mitochondria
- Mechanisms by which opening the mitochondrial ATP- sensitive 'K POT. +' channel protects the ischemic heart
- Effect of Bcl-2 overexpression on mitochondrial structure and function
- Mitochondrial ATP-sensitive 'K POT. +' channel opening decreases reactive oxygen species generation
- Mitochondrial channels that regulate cell viability
- Mitochondrial permeability transition is delayed by ATP-sensitive 'K POT. +' channel ('Mitok IND. ATP') opening
- Protection against ischemic brain injury by inhibition of mitochondrial oxidative stress
- ATP-sensitive K+ channel (mitoKATP) opening protects against cellular damage preventing mitochondrial permeability transition
- Diet, mitochondria and energy metabolism
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