Evidence of environmental pollution in caprine brains obtained from a relatively unindustrialized area in nigeria.

Igado, O. O.; Olopade, J. O.; Onwuka, SK; Onwuka, A.C; Daramola, Oluwadamilola; Ajufo, U.E

doi:10.4314/ajbr.v11i3.50744

Cited by 13 publications

(25 citation statements)

References 15 publications

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“…Vanadium emission from human industrial activities has been estimated to comprise about 53% of total atmospheric vanadium (Hope 1994). A major source of vanadium toxicity remains the burning of fossil fuels in the Arabian Gulf (Haider et al 1998) and the Niger Delta region of Nigeria (Igado et al 2008) where massive incidental and or intentional burning of vanadium containing fuels results in pollution of confined ecosystems.…”

Section: Introductionmentioning

confidence: 99%

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

et al. 2010

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The second post-natal week in rat is the period of the most intense oligodendrocyte development and myelination. This period coincides with peak iron import by oligodendrocytes. During that time oligodendrocyte progenitors (OPCs) are sensitive to agents that may disturb normal iron homeostasis and assimilation of iron into these cells. One mechanism by which iron homeostasis can be disrupted is by environmental exposure to other metals. Vanadium is a transition metal, and exposure to vanadium during early brain development produces hypomyelination with variety of related neuro-behavioral phenotypes. In the current study, we investigated mechanisms of hypomyelination induced by vanadium exposure in developing rat brain. We demonstrate that both in vivo and in vitro, OPCs are more sensitive to vanadium exposure than astrocytes or mature oligodendrocytes. Vanadium exposure in OPCs resulted in increased ROS generation and increased annexinV labeling suggestive of apoptosis. Because ferritin is a major iron delivery protein for oligodendrocytes, we exposed the cells to recombinant ferritin and iron both of which exacerbated vanadium cytotoxicity, while the iron chelator desferroxamine (DFO) prevented cytotoxic/apoptotic effects of vanadium. To illustrate relationship between ferritin and vanadium, we demonstrate that vanadium exacerbated DNA nicking produced by iron-rich spleen ferritin, but not iron-poor apoferritin, resulting in a single and double strand breaks in a DNA relaxation assay. We propose that developmental exposure to vanadium interferes with normal iron assimilation into oligodendrocytes resulting in oxidative stress and apoptosis. Therefore, depletion of OPCs due to vanadium exposure in early post-natal period may be an important mechanism of vanadium-induced hypomyelination.

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Section: Introductionmentioning

confidence: 99%

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

et al. 2010

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“…Environmental pollution from fossil fuel burning and the subsequent release of finely particulate vanadium compounds in the Arabian gulf [36] and Nigeria's Niger Delta [37]has been on the increase with minimal studies done on both the short and long term effects on the brain. Hypomyelination and or myelin destruction from lipid peroxidation has been implicated in part to be responsible for the phenotypic expressions of neuromuscular and behavioral deficits seen in vanadium toxicosis [38].…”

Section: Introductionmentioning

confidence: 99%

Gene–environment interactions: Neurodegeneration in non-mammals and mammals

Aschner

Levin

Suñol³

et al. 2010

NeuroToxicology

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The understanding of how environmental exposures interact with genetics in central nervous system dysfunction has gained great momentum in the last decade. Seminal findings have been uncovered in both mammalian and non-mammalian model in large result of the extraordinary conservation of both genetic elements and differentiation processes between mammals and non-mammalians. Emerging model organisms, such as the nematode and zebrafish have made it possible to assess the effects of small molecules rapidly, inexpensively, and on a miniaturized scale. By combining the scale and throughput of in vitro screens with the physiological complexity and traditional animal studies, these models are providing relevant information on molecular events in the etiology of neurodegenerative disorders. The utility of these models is largely driven by the functional conservation seen between them and higher organisms, including humans so that knowledge obtained using non-mammalian model systems can often provide a better understanding of equivalent processes, pathways, and mechanisms in man. Understanding the molecular events that trigger neurodegeneration has also greatly relied upon the use of tissue culture models.The purpose of this summary is to provide-state-of-the-art review of recent developments of nonmammalian experimental models and their utility in addressing issues pertinent to neurotoxicity (Caenorhabditis elegans and Danio rerio). The synopses by Aschner and Levin summarize how Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeurotoxicology. Author manuscript; available in PMC 2011 September 1. C. Elegans as an Alternative Model in Toxicology Caenorhabditis elegans in Neurotoxicology StudiesThe search for experimental models that allow live in vivo analysis in the toxicological field has led to the use of several invertebrate organisms. Caenorhabditis elegans (C. elegans) has demonstrated great advantages in providing insights into the mechanisms of toxicity and neuronal injury. The codification of the complete genome revealed the extraordinary conservation of its genome with mammals (60-80% homology) [1] and studies indicating that worms and mammals share similar biosynthetic and metabolic pathways provide justification for its relevance in the toxicological field.C. elegans has a small size (adults are ~1 mm long), ease of maintenance, ability to be frozen and stored, speedy generation time (3 days), short life span, and large brood size (>300 progeny per hermaphrodite). All these features provide a limitless supply of worms for cell...

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“…A previous study of trace elements in goat brains from an undosed population included measurements of Pb (Igado et al, 2008). In that study, atomic absorption spectrometry (AAS) was used to determine Pb content in the brains of 15 West African Dwarf goats from an unindustrialized area.…”

Section: Accumulation Of Pb In the Brain Of The Undosed Caprinementioning

confidence: 99%

“…Similarly, in human studies, because brain tissues are a precious commodity, frequently only small portions of material from select regions may be available for analysis (Andrási et al, 1990(Andrási et al, , 1995(Andrási et al, , 1999Grandjean, 1978;Rajan et al, 1997). To date, only one other apparent study examined distributions of Pb and other elements including vanadium, copper, iron, molybdenum, zinc, and aluminum in caprine brains (Igado et al, 2008). Igado et al (2008) determined interregional metal contents in 5 brain regions from 15 undosed goats that would have only been exposed to Pb through their natural environment in an unindustrialized, rural setting.…”

mentioning

confidence: 96%

“…To date, only one other apparent study examined distributions of Pb and other elements including vanadium, copper, iron, molybdenum, zinc, and aluminum in caprine brains (Igado et al, 2008). Igado et al (2008) determined interregional metal contents in 5 brain regions from 15 undosed goats that would have only been exposed to Pb through their natural environment in an unindustrialized, rural setting. Despite numerous studies that explored Pb accumulation from normal and pathological brains in animal models and humans, there is still little understanding related to brain Pb distribution (Zoeger et al, 2005).…”

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confidence: 99%

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Regional Distribution and Accumulation of Lead in Caprine Brain Tissues Following a Long-Term Oral Dosing Regimen

Steuerwald

Blaisdell

Geraghty

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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It is well known that the brain is a key target organ for lead (Pb)-induced toxicity, with exposure potentially resulting in numerous adverse neurological effects. However, information on the distribution and accumulation of Pb within different brain regions is scarce. In this study, Pb uptake and accumulation were characterized in brain and related tissues obtained from a convenience sample of goats dosed with Pb. Tissues were harvested postmortem from 10 animals (9 dosed and 1 undosed) that are used to produce blood Pb pools for the New York State Department of Health's Proficiency Testing program. Whole brains were subdivided into 14 distinct anatomical regions to explore interregional differences. Related tissues included the olfactory epithelium and spinal cord. Where sufficient tissue mass permitted, further subdivision into smaller sections was carried out to examine intraregional Pb variability. Determination of Pb content in these tissues was accomplished using inductively coupled plasma mass spectrometry (ICP-MS), with accuracy assessed using reference materials certified for Pb. Lead content (dry weight) varied from <10 ng/g, that is, below the method detection limit, to as much as 4.45 × 10(4) ng/g Pb. Olfactory epithelium Pb content was several orders of magnitude greater than found in other regions analyzed. Enrichment of Pb was also observed in the olfactory bulb and choroid plexus. Data for each region analyzed were pooled from all goats to identify regions with the greatest propensity for Pb accumulation. Data related to Pb content were also assessed individually within each goat and significant differences in Pb content between regions were determined.

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Evidence of environmental pollution in caprine brains obtained from a relatively unindustrialized area in nigeria.

Cited by 13 publications

References 15 publications

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

Gene–environment interactions: Neurodegeneration in non-mammals and mammals

Regional Distribution and Accumulation of Lead in Caprine Brain Tissues Following a Long-Term Oral Dosing Regimen

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