Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-coa dehydrogenases (2013)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Subjects: BIOQUÍMICA; MITOCÔNDRIAS
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Program and Abstracts
- Conference titles: Antioxidants and Redox Process in Health Bilateral Meeting Brazil-Japan
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ABNT
CARDOSO, Ariel e KAKIMOTO, Pamela A. H. B e KOWALTOWSKI, Alicia Juliana. Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-coa dehydrogenases. 2013, Anais.. São Paulo: SBBq, 2013. . Acesso em: 01 maio 2024. -
APA
Cardoso, A., Kakimoto, P. A. H. B., & Kowaltowski, A. J. (2013). Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-coa dehydrogenases. In Program and Abstracts. São Paulo: SBBq. -
NLM
Cardoso A, Kakimoto PAHB, Kowaltowski AJ. Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-coa dehydrogenases. Program and Abstracts. 2013 ;[citado 2024 maio 01 ] -
Vancouver
Cardoso A, Kakimoto PAHB, Kowaltowski AJ. Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-coa dehydrogenases. Program and Abstracts. 2013 ;[citado 2024 maio 01 ] - 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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