Deactivation of mitochondrial complex I after hypoxia-ischemia in the immature brain.
A/D transition
Ischemia
immature brain
mitochondrial complex I
reactive oxygen species
Journal
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
ISSN: 1559-7016
Titre abrégé: J Cereb Blood Flow Metab
Pays: United States
ID NLM: 8112566
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
pubmed:
10
4
2018
medline:
27
5
2020
entrez:
10
4
2018
Statut:
ppublish
Résumé
Mortality from perinatal hypoxic-ischemic (HI) brain injury reached 1.15 million worldwide in 2010 and is also a major factor for neurological disability in infants. HI directly influences the oxidative phosphorylation enzyme complexes in mitochondria, but the exact mechanism of HI-reoxygenation response in brain remains largely unresolved. After induction of HI-reoxygenation in postnatal day 10 rats, activities of mitochondrial respiratory chain enzymes were analysed and complexome profiling was performed. The effect of conformational state (active/deactive (A/D) transition) of mitochondrial complex I on H
Identifiants
pubmed: 29629602
doi: 10.1177/0271678X18770331
pmc: PMC6727140
doi:
Substances chimiques
Reactive Oxygen Species
0
Hydrogen Peroxide
BBX060AN9V
Electron Transport Complex I
EC 7.1.1.2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1790-1802Subventions
Organisme : Medical Research Council
ID : MR/L007339/1
Pays : United Kingdom
Organisme : NINDS NIH HHS
ID : R01 NS095692
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS083425
Pays : United States
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