ArticleRedox biology2015
Nitric oxide induces hypoxia ischemic injury in the neonatal brain via the disruption of neuronal iron metabolism.
Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Subchronic comparative assessment of graded ferrous sulfate doses on biochemical, histological, and multiorgan micromorphological changes in wistar rats.Open veterinary journal · 2026Article
- Ferroptosis in Neonatal Hypoxic-Ischemic Encephalopathy: Mechanisms and the Therapeutic Potential of Vitamin D/VDR Signaling.Cellular and molecular neurobiology · 2025Review
- Biochemical properties of molybdenum cofactor isolated from fish liver.Fish physiology and biochemistry · 2025Article
- Ginsenoside Rg1 mitigates cerebral ischaemia/reperfusion injury in mice by inhibiting autophagy through activation of mTOR signalling.Acta pharmacologica Sinica · 2024Article
- Cannabidiol effectively prevents oxidative stress and stabilizes hypoxia-inducible factor-1 alpha (HIF-1α) in an animal model of global hypoxia.Scientific reports · 2024Article
- Research progress of absorbable stents.International journal of medical sciences · 2024Review
- Advances in Ferritin Physiology and Possible Implications in Bacterial Infection.International journal of molecular sciences · 2023Review
- Astrocytes mediate long-lasting synaptic regulation of ventral tegmental area dopamine neurons.Nature neuroscience · 2022Article
- Advances in the development of biodegradable coronary stents: A translational perspective.Materials today. Bio · 2022Review
- Ultrastructural Changes in the Penumbra of the Local Cerebral Infarction in Rats.Bulletin of experimental biology and medicine · 2022Article
- Nitric oxide and thyroid carcinoma: A review.Frontiers in endocrinology · 2022Review
- Emerging Mechanisms and Disease Implications of Ferroptosis: Potential Applications of Natural Products.Frontiers in cell and developmental biology · 2021Review
- How to Improve the Antioxidant Defense in Asphyxiated Newborns-Lessons from Animal Models.Antioxidants (Basel, Switzerland) · 2020Review
- Inhaled Gases for Neuroprotection of Neonates: A Review.Frontiers in pediatrics · 2019Review
- Altered Neural Networks in the Papez Circuit: Implications for Cognitive Dysfunction after Cerebral Ischemia.Journal of Alzheimer's disease : JAD · 2019Review
- Mechanism and Treatment Related to Oxidative Stress in Neonatal Hypoxic-Ischemic Encephalopathy.Frontiers in molecular neuroscience · 2019Review
- Iron Metabolism and Brain Development in Premature Infants.Frontiers in physiology · 2019Review
- Roles of Nitric Oxide Synthase Isoforms in Neurogenesis.Molecular neurobiology · 2018Review
- Arctic ground squirrel resist peroxynitrite-mediated cell death in response to oxygen glucose deprivation.Free radical biology & medicine · 2017Article
- Oxidative stress and endoplasmic reticulum (ER) stress in the development of neonatal hypoxic-ischaemic brain injury.Biochemical Society transactions · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We have recently shown that increased hydrogen peroxide (H2O2) generation is involved in hypoxia-ischemia (HI)-mediated neonatal brain injury. H2O2 can react with free iron to form the hydroxyl radical, through Fenton Chemistry. Thus, the objective of this study was to determine if there was a role for the hydroxyl radical in neonatal HI brain injury and to elucidate the underlying mechanisms. Our data demonstrate that HI increases the deposition of free iron and hydroxyl radical formation, in both P7 hippocampal slice cultures exposed to oxygen-glucose deprivation (OGD), and the neonatal rat exposed to HI. Both these processes were found to be nitric oxide (NO) dependent. Further analysis demonstrated that the NO-dependent increase in iron deposition was mediated through increased transferrin receptor expression and a decrease in ferritin expression. This was correlated with a reduction in aconitase activity. Both NO inhibition and iron scavenging, using deferoxamine administration, reduced hydroxyl radical levels and neuronal cell death. In conclusion, our results suggest that increased NO generation leads to neuronal cell death during neonatal HI, at least in part, by altering iron homeostasis and hydroxyl radical generation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.