Vanadium And Brain

[allan]

Search Terms: Vanadium and Brain http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed

1: Neurochem Res. 2004 Jul;29(7):1365-9.

Nigrostriatal modifications after vanadium inhalation: an immunocytochemical and cytological approach.

National University of Mexico, Mexico City.

Vanadium (V) has increased in the air as a component of suspended particles originated from fuel combustion. In this report, a model of inhaled V in mice was implemented to identify the effect that V has in the corpus striatum and substantia nigra, structures with high concentrations of dopamine and scarce antioxidants burden. Mice inhaled 0.02 M V2O5 1 h twice a week and were sacrificed at points from 1 to 8 weeks after inhalation, perfused, and processed for Golgi method and for tyroxine hidroxylase (TH) inmunocytochemistry. Cytological analysis consisted in counting the number of dendritic spines in 20 medium-size spiny neurons and the number of TH immunoreactive neurons in the substatia nigra pars compacta. Dendritic spine density decreased drastically after V exposure; the same was observed with the TH-positive neurons, which decreased in a time-dependent mode. No previous morphological studies about V and nervous system have been reported. The decrease in spine density and in TH-positive neurons might have functional repercussions that should be studied because the trend of this element in the atmosphere is to increase.

PMID: 15202766 [PubMed - indexed for MEDLINE]

Search Terms: vanadium AND brain http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed

1: Toxicol Pathol. 2003 Sep-Oct;31(5):524-38.

DNA damage in nasal and brain tissues of canines exposed to air pollutants is associated with evidence of chronic brain inflammation and neurodegeneration.

Environmental Pathology Program, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA. liliancalderon888@hotmail.com

Acute, subchronic, or chronic exposures to particulate matter (PM) and pollutant gases affect people in urban areas and those exposed to fires, disasters, and wars.

Respiratory tract inflammation, production of mediators of inflammation capable of reaching the brain, systemic circulation of PM, and disruption of the nasal respiratory and olfactory barriers are likely in these populations. DNA damage is crucial in aging and in age-associated diseases such as Alzheimer's disease.

We evaluated ... healthy dogs naturally exposed to urban pollution in Mexico City.

Nickel (Ni) and vanadium (V) were measured by inductively coupled plasma mass spectrometry (ICP-MS).

Forty mongrel dogs, ages 7 days-10 years were studied (14 controls from Tlaxcala and 26 exposed to urban pollution in South West Metropolitan Mexico City (SWMMC)).

Nasal respiratory and olfactory epithelium were found to be early pollutant targets.

Olfactory bulb and hippocampal AP sites were significantly higher in exposed than in control age matched animals. Ni and V[anadium] were present in a gradient from olfactory mucosa > olfactory bulb > frontal cortex.

Exposed dogs had (a) nuclear neuronal NFkappaB p65, (b) endothelial, glial and neuronal iNOS, © endothelial and glial COX2, (d) ApoE in neuronal, glial and vascular cells, and (e) APP and beta amyloid(1-42) in neurons, diffuse plaques (the earliest at age 11 months), and in subarachnoid blood vessels.

Increased AP sites and the inflammatory and stress protein brain responses were early and significant in dogs exposed to urban pollution.

Oil combustion PM-associated metals Ni and Vanadium were detected in the brain. There was an acceleration of Alzheimer's-type pathology in dogs chronically exposed to air pollutants. Respiratory tract inflammation and deteriorating olfactory and respiratory barriers may play a role in the observed neuropathology. These data suggest that Alzheimer's disease may be the sequela of air pollutant exposures and the resulting systemic inflammation.

PMID: 14692621 [PubMed - indexed for MEDLINE]