ArticleOxidative medicine and cellular longevity2016
An Abnormal Nitric Oxide Metabolism Contributes to Brain Oxidative Stress in the Mouse Model for the Fragile X Syndrome, a Possible Role in Intellectual Disability.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Combined Restraint Stress and Metal Exposure Paradigms in Rats: Unravelling Behavioural and Neurochemical Perturbations.Molecular neurobiology · 2025Article
- Apocynin, a Selective NADPH Oxidase (Nox2) Inhibitor, Ameliorates Behavioural and Learning Deficits in the Fragile X Syndrome Mouse Model.Biomedicines · 2024Article
- Mitochondrial dysfunction in Fragile X syndrome and Fragile X-associated tremor/ataxia syndrome: prospect use of antioxidants and mitochondrial nutrients.Molecular biology reports · 2024Review
- Effects of a Floor Hockey Intervention on Motor Proficiency, Physical Fitness, and Adaptive Development in Youths with Mild Intellectual Disabilities.International journal of environmental research and public health · 2021Article
- How Robust is the Evidence for a Role of Oxidative Stress in Autism Spectrum Disorders and Intellectual Disabilities?Journal of autism and developmental disorders · 2021Review
- Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2021Article
- Oxidative Stress in Cognitive and Epigenetic Aging: A Retrospective Glance.Frontiers in molecular neuroscience · 2020Review
- A pilot study on machine learning approach to delineate metabolic signatures in intellectual disability.International journal of developmental disabilities · 2019Article
- Reduced mitochondrial fusion and Huntingtin levels contribute to impaired dendritic maturation and behavioral deficits in Fmr1-mutant mice.Nature neuroscience · 2019Article
- Impaired oxidative stress response characterizes HUWE1-promoted X-linked intellectual disability.Scientific reports · 2017Article
- Fragile X Mental Retardation Protein Restricts Small Dye Iontophoresis Entry into Central Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFragile X syndrome is the most common genetic cause of mental disability. Although many research has been performed, the mechanism underlying the pathogenesis is unclear and needs further investigation. Oxidative stress played major roles in the syndrome. The aim was to investigate the nitric oxide metabolism, protein nitration level, the expression of NOS isoforms, and furthermore the activation of the nuclear factor NF-κB-p65 subunit in different brain areas on the fragile X mouse model.
methodsThis study involved adult male Fmr1-knockout and wild-type mice as controls. We detected nitric oxide metabolism and the activation of the nuclear factor NF-κBp65 subunit, comparing the mRNA expression and protein content of the three NOS isoforms in different brain areas.
resultsFmr1-KO mice showed an abnormal nitric oxide metabolism and increased levels of protein tyrosine nitrosylation. Besides that, nuclear factor NF-κB-p65 and inducible nitric oxide synthase appeared significantly increased in the Fmr1-knockout mice. mRNA and protein levels of the neuronal nitric oxide synthase appeared significantly decreased in the knockout mice. However, the epithelial nitric oxide synthase isoform displayed no significant changes.
conclusionsThese data suggest the potential involvement of an abnormal nitric oxide metabolism in the pathogenesis of the fragile X syndrome.
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