Oxygen and glucose deprivation induces mitochondrial dysfunction and oxidative stress in neurones but not in astrocytes in primary culture

A Almeida, M Delgado‐Esteban… - Journal of …, 2002 - Wiley Online Library
In order to investigate the potential neuroprotective role played by glucose metabolism
during brain oxygen deprivation, the susceptibility of cultured neurones and astrocytes to 1 h …

The oxygen free radicals originating from mitochondrial complex I contribute to oxidative brain injury following hypoxia–ischemia in neonatal mice

ZV Niatsetskaya, SA Sosunov… - Journal of …, 2012 - Soc Neuroscience
Oxidative stress and Ca2+ toxicity are mechanisms of hypoxic–ischemic (HI) brain injury.
This work investigates if partial inhibition of mitochondrial respiratory chain protects HI brain …

Mitochondrial respiratory chain and free radical generation in stroke

MA Moro, A Almeida, JP Bolaños, I Lizasoain - Free Radical Biology and …, 2005 - Elsevier
Being the second most common cause of death in the industrial countries and one of the
major causes of death and disability, stroke has a great effect on public health and is the …

[HTML][HTML] Selenium preserves mitochondrial function, stimulates mitochondrial biogenesis, and reduces infarct volume after focal cerebral ischemia

SL Mehta, S Kumari, N Mendelev, PA Li - BMC neuroscience, 2012 - Springer
Background Mitochondrial dysfunction is one of the major events responsible for activation
of neuronal cell death pathways during cerebral ischemia. Trace element selenium has …

Specific caspase pathways are activated in the two stages of cerebral infarction

A Benchoua, C Guégan, C Couriaud… - Journal of …, 2001 - Soc Neuroscience
Necrosis and apoptosis have been initially identified as two exclusive pathways for cell
death. In acute brain lesions, such as focal ischemia, this binary scheme is challenged by …

Metabolic stages, mitochondria and calcium in hypoxic/ischemic brain damage

T Kristián - Cell calcium, 2004 - Elsevier
Cerebral hypoxia/ischemia leads to mitochondrial dysfunction due to lack of oxygen leaving
the glycolytic metabolism as a main pathway for ATP production. Inhibition of mitochondrial …

Mitochondrial nitric oxide synthase: a ubiquitous regulator of oxidative phosphorylation?

TE Bates, A Loesch, G Burnstock, JB Clark - Biochemical and biophysical …, 1996 - Elsevier
In this article we demonstrate the immunocytochemical localization of nitric oxide synthase
in mitochondria isolated from heart, skeletal muscle, and kidney, using a monoclonal …

Brain ischemia/reperfusion injury and mitochondrial complex I damage

A Galkin - Biochemistry (moscow), 2019 - Springer
Ischemic stroke and neonatal hypoxic-ischemic encephalopathy are two of the leading
causes of disability in adults and infants. The energy demands of the brain are provided by …

Critical role of flavin and glutathione in complex I–mediated bioenergetic failure in brain ischemia/reperfusion injury

A Kahl, A Stepanova, C Konrad, C Anderson… - Stroke, 2018 - Am Heart Assoc
Background and Purpose—Ischemic brain injury is characterized by 2 temporally distinct but
interrelated phases: ischemia (primary energy failure) and reperfusion (secondary energy …

Mitochondria and reactive oxygen and nitrogen species in neurological disorders and stroke: therapeutic implications

JP Bolaños, MA Moro, I Lizasoain, A Almeida - Advanced drug delivery …, 2009 - Elsevier
Mitochondria represent both the main source and target of reactive oxygen and nitrogen
species (RONS). In view of the large energy expenditure made by neurons during …