| Autor: |
Oscar A. Mejía-García, Vianey Rodríguez-Lara, Rocío Tron-Alvarez, Leonardo Reynoso-Erazo, Ana Luisa Gutierrez-Valdez, Enrique Montiel-Flores, Jesús Espinosa-Villanueva, Maria Rosa Avila-Costa, Claudia Dorado-Martínez, José Luis Ordoñez-Librado |
| Rok vydání: |
2022 |
| Předmět: |
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| Zdroj: |
Neurotoxicity-New Advances [Working Title] |
| DOI: |
10.5772/intechopen.100468 |
| Popis: |
Vanadium (V), a widely distributed transition metal, has been considered toxic, which depends on the valence of the compound. V pentoxide (V2O5) is considered the most harmful. Its long-term exposure produces neurotoxicity. Mice exposed to inhaled V2O5 displayed less tubulin+ in testicular cells and dendritic spines loss, cell death, and CA1 neuropil modifications, considered as the result of V interaction with the cytoskeleton, which made us suppose that V2O5 inhalation could initiate CA1 cell alterations comparable to what happen in the brains of Alzheimer disease (AD) patients. This study intends to demonstrate pyramidal CA1 cytoskeletal changes in rats which inhaled V2O5. Twenty rats were exposed to V2O5 0.02 M one hour, three times a week for several months. Our findings showed that V2O5-exposed rats had cell death that reached 56,57% after six months; we also observed collapsed strong argyrophilic nuclei and characteristic flame-shaped somas in all V2O5-exposed animals hippocampus CA1 compared to controls. We also found somatodendritic deformations. Neurite’s cytoskeleton exhibited visible thickening and nodosities and prominent dendritic spine loss. Our results demonstrate that V2O5 induces AD-like cell death with evident cytoskeletal and synaptic alterations. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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