Hippocampal cell alterations induced by the inhalation of vanadium pentoxide (V2O5) promote memory deterioration

Avila-Costa, Marı́a Rosa; Fortoul, Teresa I.; Niño-Cabrera, Geraldine; Colı́n-Barenque, Laura; Bizarro-Nevares, Patrícia; Gutiérrez-Valdez, Ana Luisa; Ordóñez-Librado, José Luis; Rodríguez-Lara, Vianey; Mussali-Galante, Patricia; Díaz-Bech, Patricia; Anaya-Martı́nez, Verónica

doi:10.1016/j.neuro.2006.04.001

Cited by 65 publications

(39 citation statements)

References 21 publications

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“…The increase in MMP-2 might also be associated with the increase in cell death observed in the hippocampus as mentioned above (Avila-Costa et al, 2006).…”

Section: Discussionmentioning

confidence: 74%

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Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation

Colı́n-Barenque

Martínez-Hernández

Baiza-Gutman

et al. 2007

J of Applied Toxicology

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Vanadium (V) derivatives are well-known environmental pollutants and its toxicity has been related with oxidative stress. Toxicity after vanadium inhalation on the substantia nigra, corpus striatum, hippocampus and ependymal epithelium was reported previously. The purpose of this study was to analyse the role of matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) in the changes observed in brain tissue after chronic V inhalation. Mice were exposed to vaporized, vanadium pentoxide 0.02 m in deionized water for 1 h twice a week, and killed at 1 h, 1, 2 and 4 weeks after exposure. The brain was removed and the olfactory bulb, prefrontal cortex, striatum and hippocampus were dissected and the MMP content was obtained by zymography. The results showed that MMP-9 increased in all the structures at the end of the exposure, although in the hippocampus this increment was evident after 1 week of exposure. When MMP-2 was analysed in the olfactory bulb and prefrontal cortex it remained unchanged throughout the whole exposure, while in the hippocampus it increased at week 4, while in the striatum MMP-2 increased from the second week only, through the whole experiment. These results demonstrate that V increased MMPs in different structures of the CNS and this change might be associated with the previously reported modifications, such as dendritic spine loss and neuronal cell death. The modifications in MMPs could be related with blood-brain barrier (BBB) disruption which was reported previously. Oxidative stress might also be involved in the activation of these gelatinases as part of the different mechanisms which take place in V toxicity in the CNS.

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“…The increase in MMP-2 might also be associated with the increase in cell death observed in the hippocampus as mentioned above (Avila-Costa et al, 2006).…”

Section: Discussionmentioning

confidence: 74%

“…necrosis in the hippocampus, resulting in impairment of spatial memory (Avila-Costa et al, 2006). Neuronal depletion in the substantia nigra and a decrease in the number of dendritic spines in the medium-size spiny neurons in the striatum of exposed mice were also reported (Avila-Costa et al, 2004).…”

mentioning

confidence: 99%

Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation

Colı́n-Barenque

Martínez-Hernández

Baiza-Gutman

et al. 2007

J of Applied Toxicology

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“…In humans, exposure to vanadium results in neurobehavioral alteration, such as the reduced functions in emotion, cognition, and motor accuracy [11,12]. In adult rats, vanadium exposure causes neuropathological lesions in hippocampal neurons [13], as well as oxidative stress and demyelination in the cerebellum [14,15]. Because vanadium is present in breast milk and easily passes the blood brain barrier, it could cause developmental neurotoxicity in the exposed neonatal animals [16].…”

Section: Introductionmentioning

confidence: 99%

Recovery of motor coordination after exercise is correlated to enhancement of brain-derived neurotrophic factor in lactational vanadium-exposed rats

Wang

Lin

2015

Neuroscience Letters

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“…Also, the morphological alterations of neurons and astroglial cells in adult rat central nervous system after vanadium exposure was reported [23]. Vanadium can exert neurotoxic effects in dopaminergic neuronal cells via caspase-3-dependent PKCδ cleavage [24]. Vanadium exposure through lactation would induce neurotoxicity in rat developing CNS [25].…”

Section: Discussionmentioning

confidence: 99%

Vanadium exposure-induced neurobehavioral alterations among Chinese workers

Zhou

Zhang

et al. 2013

NeuroToxicology

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Vanadium-containing products are manufactured and widely used in the modern industry. Yet the neurobehavioral toxicity due to occupational exposure to vanadium remained elusive. This cross-sectional study was designed to examine the neurotoxic effects of occupational vanadium exposure. A total of 463 vanadium-exposed workers (exposed group) and 251 non-exposed workers (control group) were recruited from a Steel and Iron Group in Sichuan, China. A WHO-recommended neurobehavioral core test battery (NCTB) and event-related auditory evoked potentials test (P300) were used to assess the neurobehavioral functions of all study subjects. A general linear model was used to compare outcome scores between the two groups while controlling for possible confounders. The exposed group showed a statistically significant neurobehavioral alteration more than the control group in the NCTB tests. The exposed workers also exhibited an increased anger-hostility, depression-dejection and fatigue-inertia on the profile of mood states (p<0.05). Performances in the Simple Reaction Time, Digit Span, Benton Visual Retention and Pursuit Aiming were also poorer among exposed workers as compared to unexposed control workers(p<0.05). Some of these poor performances in tests were also significantly related to workers’ exposure duration. P300 latencies were longer in the exposed group than in the control (p<0.05). Longer mean reaction times and more counting errors were also found in the exposed workers (p<0.05). Given the findings of our study and the limitations of neurobehavioral workplace testing, we found evidence of altered neurobehavioral outcomes by occupational exposure to vanadium.

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Hippocampal cell alterations induced by the inhalation of vanadium pentoxide (V2O5) promote memory deterioration

Cited by 65 publications

References 21 publications

Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation

Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation

Recovery of motor coordination after exercise is correlated to enhancement of brain-derived neurotrophic factor in lactational vanadium-exposed rats

Vanadium exposure-induced neurobehavioral alterations among Chinese workers

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