title: Neurobehavioral and cytotoxic effects of vanadium during oligodendrocyte maturation: a protective role for erythropoietin.
abstract: Vanadium exposure has been known to lead to lipid peroxidation, demyelination and oligodendrocytes depletion. We investigated behaviour and glial reactions in juvenile mice after early neonatal exposure to vanadium, and examined the direct effects of vanadium in oligodendrocyte progenitor cultures from embryonic mice. Neonatal pups exposed to vanadium via lactation for 15 and 22 days all had lower body weights. Behavioural tests showed in most instances a reduction in locomotor activity and negative geotaxis. Brain analyses revealed astrocytic activation and demyelination in the vanadium exposed groups compared to the controls. In cell culture, exposure of oligodendrocytes to 300 μM sodium metavanadate significantly increased cell death. Expression of the oligodendrocyte specific proteins, 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) and oligodendrocyte specific protein (OSP/Claudin) were reduced upon vanadium treatment while simultaneous administration of erythropoietin (EPO; 4-12 U/ml) counteracted vanadium-toxicity. The data suggest that oligodendrocyte damage may explain the increased vulnerability of the juvenile brain to vanadium and support a potential for erythropoietin as a protective agent against vanadium-toxicity during perinatal brain development and maturation.
authors.affiliation: Department of Veterinary Anatomy, University of Ibadan, Nigeria; Department of Veterinary Anatomy, Federal University of Agriculture, Abeokuta, Nigeria. Electronic address: drmustyplato@yahoo.co.uk.
authors.forename: Oluwaseun
authors.initials: O
authors.lastname: Mustapha
authors.affiliation: Department of Veterinary Anatomy, University of Ibadan, Nigeria. Electronic address: bankoleoke@yahoo.com.
authors.forename: Bankole
authors.initials: B
authors.lastname: Oke
authors.affiliation: Department of Neurosurgery, University of Würzburg, Josef-Schneider Strasse 11, 97080 Würzburg, Germany. Electronic address: nils.offen@med.lu.se.
authors.forename: Nils
authors.initials: N
authors.lastname: Offen
authors.affiliation: Department of Neurosurgery, University of Würzburg, Josef-Schneider Strasse 11, 97080 Würzburg, Germany. Electronic address: siren.a@ukw.de.
authors.forename: Anna-Leena
authors.initials: AL
authors.lastname: Sirén
authors.affiliation: Department of Veterinary Anatomy, University of Ibadan, Nigeria; Department of Neurosurgery, University of Würzburg, Josef-Schneider Strasse 11, 97080 Würzburg, Germany. Electronic address: jkayodeolopade@yahoo.com.
authors.forename: James
authors.initials: J
authors.lastname: Olopade
mesh_terms: D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases / Q000378:metabolism; D000818:Animals; D050256:Antimitotic Agents / Q000633:toxicity*; D001007:Anxiety / Q000188:drug therapy; D001522:Behavior, Animal / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D057167:Claudins / Q000378:metabolism; D004921:Erythropoietin / Q000494:pharmacology*; D005106:Exploratory Behavior / Q000187:drug effects; D005260:Female; D005904:Glial Fibrillary Acidic Protein; D051379:Mice; D008810:Mice, Inbred C57BL; D009043:Motor Activity / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009498:Neurotoxins / Q000633:toxicity*; D009836:Oligodendroglia / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D014639:Vanadium / Q000633:toxicity*
chemical_list: D050256:Antimitotic Agents; D057167:Claudins; C492354:Cldn11 protein, mouse; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D009498:Neurotoxins; C528900:glial fibrillary astrocytic protein, mouse; D014639:Vanadium; D004921:Erythropoietin; D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases
keywords: Demyelination; Neuroprotection; Neurotoxicity; Oligodendrocyte depletion