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Alzheimer-like cell death after vanadium pentoxide inhalation
Enrique Montiel-Flores1, Oscar A Mejía-García1, Jose Luis Ordoñez-Librado1
1Neuromorphology Lab, Facultad de Estudios Superiores Iztacala, UNAM, Av. de los Barrios 1, Los Reyes Iztacala, Tlalnepantla, Edo. Mex., 54090, Mexico.
Heliyon
|September 2, 2021
Summary
Vanadium pentoxide (V2O5) inhalation causes significant neuronal death and cytoskeletal damage in the rat hippocampus. These V2O5-induced changes mimic Alzheimer
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Vanadium (V) toxicity is oxidation-state dependent, with vanadium pentoxide (V2O5) being highly toxic to cells.
- Previous studies link V2O5 exposure to motor and learning deficits, oxidative stress in the brain, and cytoskeletal disruptions in reproductive cells.
- Inhaled V2O5 has been associated with neuronal damage, including loss of dendritic spines and hippocampus alterations, suggesting potential parallels with Alzheimer disease.
Purpose of the Study:
- To investigate the effects of V2O5 inhalation on cytoskeletal alterations in the pyramidal hippocampal CA1 region of rats.
- To determine if V2O5 exposure induces neuronal death in the hippocampus, similar to that observed in Alzheimer disease.
Main Methods:
- Male Wistar rats were exposed to inhaled 0.02 M V2O5 for one hour, twice weekly, over two and six months.
- Cytoskeletal alterations in the hippocampal CA1 region were analyzed using Bielschowsky staining.
- Quantification of neuronal death and observation of morphological changes in neurons, axons, and dendrites were performed.
Main Results:
- Six months of V2O5 inhalation resulted in 56.57% dead neurons in the hippocampal CA1 region.
- V2O5-exposed rats exhibited collapsed neuronal somas, flame-shaped structures, and somatodendritic distortions.
- Significant alterations in axons and dendrites were observed, including thickening, nodosities, and disruption of linear cytoskeletal protein traces.
Conclusions:
- Inhalation of V2O5 induces significant neuronal death in the rat hippocampus.
- V2O5 exposure causes profound cytoskeletal alterations, including distortions and disruptions.
- The observed V2O5-induced neuropathology resembles Alzheimer disease, suggesting V2O5 as a potential neurotoxic agent contributing to Alzheimer-like pathology.
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