Nitric oxide, hypoxia and brain inflammation.
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Summary
It is found that NO from an NO donor or glial inducible NOS (nitric oxide synthase) highly sensitizes neurons to hypoxia-induced death, probably via the NO-oxygen competition at cytochrome oxidase.
- Type
- article
- Published
- 2004-11-01
- Cited by
- 35
- References
- 15
- OpenAlex
- https://openalex.org/W1999723741
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:31532211
Keywords
Cytochrome c oxidase, Nitric oxide, Nitric oxide synthase, Hypoxia (environmental), Excitotoxicity
References
- Oxygen conformance of cellular respiration. A perspective of mitochondrial physiology.
- Inflammatory Neurodegeneration Mediated by Nitric Oxide from Activated Glia-Inhibiting Neuronal Respiration, Causing Glutamate Release and Excitotoxicity
- Transcellular regulation of cell respiration by nitric oxide generated by activated macrophages
- Expression of the inducible form of nitric oxide synthase by reactive astrocytes after transient global ischemia.
- Enhanced glial activation and expression of specific CNS inflammation-related molecules in aged versus young rats following cortical stab injury.
- Inducible Nitric Oxide Synthase Expression in Cerebrovascular Smooth Muscle and Neutrophils after Traumatic Brain Injury in Immature Rats1
- Regional Energy Balance in Rat Brain After Transient Forebrain Ischemia
- A possible mechanism for the hypoxia-hypoglycemia-induced release of excitatory amino acids from cultured hippocampal astrocytes
- Nanomolar concentrations of nitric oxide reversibly inhibit synaptosomal respiration by competing with oxygen at cytochrome oxidase
- Tissue oxygen tension and brain sensitivity to hypoxia.
- Precipitants of brain infarction. Roles of preceding infection/inflammation and recent psychological stress.
- Glycolysis can prevent non-synaptic excitatory amino acid release during hypoxia.
- Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain.
- Cytoskeletal Breakdown and Apoptosis Elicited by NO Donors in Cerebellar Granule Cells Require NMDA Receptor Activation
- Microglia: a sensor for pathological events in the CNS.
Cited by
- Co-Administration of Acetyl-11-Keto-β-Boswellic Acid, a Specific 5-Lipoxygenase Inhibitor, Potentiates the Protective Effect of COX-2 Inhibitors in Kainic Acid-Induced Neurotoxicity in Mice
- Effect of NOS-Compartmentalisation on Cerebral Perfusion and Oxygen Metabolism in Physiological and Pathological Conditions
- The role of hypoxia in neuroinflammatory disease
- Melatonin restores the cytochrome oxidase reactivity in the nodose ganglia of acute hypoxic rats
- Cerebrovascular Disorders: Role of Aging
- Preconditioning and post-treatment with cobalt chloride in rat model of perinatal hypoxic-ischemic encephalopathy.
- Ab initio modelling of the structure and redox behaviour of copper(I) bound to a His–His model peptide: relevance to the β-amyloid peptide of Alzheimer’s disease
- Protective role of melatonin in mitochondrial dysfunction and related disorders
- Nitric Oxide, a Powerful Clinical Therapy
- Neurobiology of Vascular Dementia
- Altered in vitro immune response to hypoxia-treated normal peritoneal fibroblasts.
- Role of melatonin in neurodegenerative diseases
- Physiological oxygen level is critical for modeling neuronal metabolism in vitro
- Melatonin in Mitochondrial Dysfunction and Related Disorders
- The basic science of Meniere's disease and endolymphatic hydrops
- Cellular bioenergetics changes in magnocellular neurons may affect copeptin expression in the late phase of sepsis.
- Prodeath or Prosurvival: Two Facets of Hypoxia Inducible Factor-1 in Perinatal Brain Injury
- Role of central NO-cGMP pathway in vasopressin and oxytocin gene expression during sepsis.
- Cleaved caspase-3 expression in hypothalamic magnocellular neurons may affect vasopressin secretion during experimental polymicrobial sepsis.
- The chemistry of Alzheimer's disease.
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