ArticleMediators of inflammation2013
JNK and NADPH oxidase involved in fluoride-induced oxidative stress in BV-2 microglia cells.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- Water Fluoridation and Birth Outcomes in California.Environmental health perspectives · 2024Article
- Fluoride promotes the secretion of inflammatory factors in microglia through NLRP3/Caspase-1/GSDMD pathway.Environmental science and pollution research international · 2024Article
- Molecular basis of fluoride toxicities: Beyond benefits and implications in human disorders.Genes & diseases · 2023Review
- Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours-A Research Hypothesis.International journal of molecular sciences · 2023Review
- Anti-neuroinflammatory of Chloroform Extract ofReports of biochemistry & molecular biology · 2022Article
- Glial Purinergic Signaling-Mediated Oxidative Stress (GPOS) in Neuropsychiatric Disorders.Oxidative medicine and cellular longevity · 2022Review
- Melatonin and Microglia.International journal of molecular sciences · 2021Review
- Fluoride Exposure Affects Glutamine Uptake in Müller Glia Cells.Neurotoxicity research · 2020Article
- ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Mechanisms of Inhibition of Excessive Microglial Activation by Melatonin.Journal of molecular neuroscience : MN · 2020Review
- Toxicity of fluoride: critical evaluation of evidence for human developmental neurotoxicity in epidemiological studies, animal experiments and in vitro analyses.Archives of toxicology · 2020Review
- The pathogenesis of endemic fluorosis: Research progress in the last 5 years.Journal of cellular and molecular medicine · 2019Review
- An Evaluation of Neurotoxicity Following Fluoride Exposure from Gestational Through Adult Ages in Long-Evans Hooded Rats.Neurotoxicity research · 2018Article
- Role of Mitogen Activated Protein Kinase Signaling in Parkinson's Disease.International journal of molecular sciences · 2018Review
- Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of autism spectrum disorders: A possible role of fluoride and aluminum.Surgical neurology international · 2018Review
- Fluoride Induces Neuroinflammation and Alters Wnt Signaling Pathway in BV2 Microglial Cells.Inflammation · 2017Article
- Enteric innervation combined with proteomics for the evaluation of the effects of chronic fluoride exposure on the duodenum of rats.Scientific reports · 2017Article
- Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain.Molecular neurobiology · 2016Article
- The History, Status, Gaps, and Future Directions of Neurotoxicology in China.Environmental health perspectives · 2016Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action of fluoride toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), and NADPH oxidase (NOX) is the major enzyme for the production of extracellular superoxide in microglia. ROS have been characterized as an important secondary messenger and modulator for various mammalian intracellular signaling pathways, including the MAPK pathways. In this study we examined ROS production and TNF- α , IL-1 β inflammatory cytokines releasing, and the expression of MAPKs in BV-2 microglia cells treated with fluoride. We found that fluoride increased JNK phosphorylation level of BV-2 cells and pretreatment with JNK inhibitor SP600125 markedly reduced the levels of intracellular O₂(·-) and NO. NOX inhibitor apocynin and iNOS inhibitor SMT dramatically decreased NaF-induced ROS and NO generations, respectively. Antioxidant melatonin (MEL) resulted in a reduction in JNK phosphorylation in fluoride-stimulated BV-2 microglia. The results confirmed that NOX and iNOS played an important role in fluoride inducing oxidative stress and NO production and JNK took part in the oxidative stress induced by fluoride and meanwhile also could be activated by ROS in fluoride-treated BV-2 cells.
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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.