ArticleNeurotoxicology2014
Vanadium exposure induces olfactory dysfunction in an animal model of metal neurotoxicity.
Article in Neurotoxicology, 2014. 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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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Modelling Olfactory Dysfunction in Rodents Through Intranasal Vanadium Exposure.Animals : an open access journal from MDPI · 2026Review
- Preclinical Evaluation of Synthetic Biology-Driven EngineeredACS synthetic biology · 2026Article
- Neurotoxic Effect of Manganese and Vanadium Co-Exposure in Animal Models of Parkinson's Disease.International journal of molecular sciences · 2026Article
- Establishment of nasal and olfactory epithelium organoids for unveiling mechanism of tissue regeneration and pathogenesis of nasal diseases.Cellular and molecular life sciences : CMLS · 2025Review
- Characterization of an olfactory system dysfunction model: a vanadium dose-effect study via nose-to-brain delivery in rats.Frontiers in neuroanatomy · 2025Article
- Manganese and Vanadium Co-Exposure Induces Severe Neurotoxicity in the Olfactory System: Relevance to Metal-Induced Parkinsonism.International journal of molecular sciences · 2024Article
- Review
- CNS-Related Effects Caused by Vanadium at Realistic Exposure Levels in Humans: A Comprehensive Overview Supplemented with Selected Animal Studies.International journal of molecular sciences · 2023Review
- Neuroecotoxicology: Effects of environmental heavy metal exposure on the brain of African giant rats and the contribution of vanadium to the neuropathology.IBRO neuroscience reports · 2022Article
- Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson's Disease.International journal of molecular sciences · 2022Review
- Environmental triggers of Parkinson's disease - Implications of the Braak and dual-hit hypotheses.Neurobiology of disease · 2022Review
- Characterization of nonmotor behavioral impairments and their neurochemical mechanisms in the MitoPark mouse model of progressive neurodegeneration in Parkinson's disease.Experimental neurology · 2021Article
- Response of Cytoprotective and Detoxifying Proteins to Vanadate and/or Magnesium in the Rat Liver: The Nrf2-Keap1 System.Oxidative medicine and cellular longevity · 2021Article
- Nervonic acid amends motor disorder in a mouse model of Parkinson's disease.Translational neuroscience · 2021Article
- The Pathopharmacological Interplay between Vanadium and Iron in Parkinson's Disease Models.International journal of molecular sciences · 2020Article
- Autonomic ganglionic injection of α-synuclein fibrils as a model of pure autonomic failure α-synucleinopathy.Nature communications · 2020Article
- Neuroprotective effect of carnosine in the olfactory bulb after vanadium inhalation in a mouse model.International journal of experimental pathology · 2018Article
- Respirable Uranyl-Vanadate-Containing Particulate Matter Derived From a Legacy Uranium Mine Site Exhibits Potentiated Cardiopulmonary Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Article
- Manganese exposure induces neuroinflammation by impairing mitochondrial dynamics in astrocytes.Neurotoxicology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiological evidence indicates chronic environmental exposure to transition metals may play a role in chronic neurodegenerative conditions such as Parkinson's disease (PD). Chronic inhalation exposure to welding fumes containing metal mixtures may be associated with development of PD. A significant amount of vanadium is present in welding fumes, as vanadium pentoxide (V2O5), and incorporation of vanadium in the production of high strength steel has become more common. Despite the increased vanadium use in recent years, the neurotoxicological effects of this metal are not well characterized. Recently, we demonstrated that V2O5 induces dopaminergic neurotoxicity via protein kinase C delta (PKCδ)-dependent oxidative signaling mechanisms in dopaminergic neuronal cells. Since anosmia (inability to perceive odors) and non-motor deficits are considered to be early symptoms of neurological diseases, in the present study, we examined the effect of V2O5 on the olfactory bulb in animal models. To mimic the inhalation exposure, we intranasally administered C57 black mice a low-dose of 182μg of V2O5 three times a week for one month, and behavioral, neurochemical and biochemical studies were performed. Our results revealed a significant decrease in olfactory bulb weights, tyrosine hydroxylase (TH) levels, levels of dopamine (DA) and its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC) and increases in astroglia of the glomerular layer of the olfactory bulb in the treatment groups relative to vehicle controls. Neurochemical changes were accompanied by impaired olfaction and locomotion. These findings suggest that nasal exposure to V2O5 adversely affects olfactory bulbs, resulting in neurobehavioral and neurochemical impairments. These results expand our understanding of vanadium neurotoxicity in environmentally-linked neurological conditions.
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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.