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
- DOI: 10.1371/journal.pone.0077088
- Subjects: MITOCÔNDRIAS; ÁCIDOS GRAXOS; BIOQUÍMICA
- Language: Inglês
- Imprenta:
- Publisher place: San Francisco
- Date published: 2013
- Source:
- Este periódico é de acesso aberto
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: gold
- Licença: cc-by
-
ABNT
CARDOSO, Ariel Rodrigues e KAKIMOTO, Pâmela 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. PLOS ONE, v. 8, n. 10, p. 1-13, 2013Tradução . . Disponível em: https://doi.org/10.1371/journal.pone.0077088. Acesso em: 19 abr. 2024. -
APA
Cardoso, A. R., 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. PLOS ONE, 8( 10), 1-13. doi:10.1371/journal.pone.0077088 -
NLM
Cardoso AR, Kakimoto PAHB, Kowaltowski AJ. Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-Coa dehydrogenases [Internet]. PLOS ONE. 2013 ; 8( 10): 1-13.[citado 2024 abr. 19 ] Available from: https://doi.org/10.1371/journal.pone.0077088 -
Vancouver
Cardoso AR, Kakimoto PAHB, Kowaltowski AJ. Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-Coa dehydrogenases [Internet]. PLOS ONE. 2013 ; 8( 10): 1-13.[citado 2024 abr. 19 ] Available from: https://doi.org/10.1371/journal.pone.0077088 - Caloric restriction protects mice against isoproterenol-induced cardiac hypertrophy by mechanisms that involve mitochondrial ATP sensitive potassium channel and modulation of redox state
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- 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
Informações sobre o DOI: 10.1371/journal.pone.0077088 (Fonte: oaDOI API)
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