Intermittent feedings promte lower body weight associated with redox imbalance in sprague-dawley rats (2012)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Subjects: MITOCÔNDRIAS; BIOQUÍMICA
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq)
- Publisher place: São Paulo
- Date published: 2012
- Source:
- Título do periódico: Program and Index
- Conference titles: Annual Meeting of the Brazilian Biochemistry and Molecular Biology Society (SBBq)
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ABNT
CHAUSSE, Bruno e CALDEIRA DA SILVA, Camille Cristine e KOWALTOWSKI, Alicia Juliana. Intermittent feedings promte lower body weight associated with redox imbalance in sprague-dawley rats. 2012, Anais.. São Paulo: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq), 2012. . Acesso em: 13 set. 2024. -
APA
Chausse, B., Caldeira da Silva, C. C., & Kowaltowski, A. J. (2012). Intermittent feedings promte lower body weight associated with redox imbalance in sprague-dawley rats. In Program and Index. São Paulo: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq). -
NLM
Chausse B, Caldeira da Silva CC, Kowaltowski AJ. Intermittent feedings promte lower body weight associated with redox imbalance in sprague-dawley rats. Program and Index. 2012 ;[citado 2024 set. 13 ] -
Vancouver
Chausse B, Caldeira da Silva CC, Kowaltowski AJ. Intermittent feedings promte lower body weight associated with redox imbalance in sprague-dawley rats. Program and Index. 2012 ;[citado 2024 set. 13 ] - 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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