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dc.contributor.authorCOCCINI Teresaen_GB
dc.contributor.authorCASTOLDI Annaen_GB
dc.contributor.authorRODA Elisaen_GB
dc.contributor.authorSARIGIANNIS DIMOSTHENISen_GB
dc.contributor.authorMANZO Luigien_GB
dc.date.accessioned2010-02-25T16:31:36Z-
dc.date.available2009-02-13en_GB
dc.date.available2010-02-25T16:31:36Z-
dc.date.created2009-02-13en_GB
dc.date.issued2008en_GB
dc.date.submitted2008-05-26en_GB
dc.identifier.citationFRESENIUS ENVIRONMENTAL BULLETIN vol. 17 no. 9b p. 1432-1438en_GB
dc.identifier.issn1018-4619en_GB
dc.identifier.urihttp://publications.jrc.ec.europa.eu/repository/handle/JRC45634-
dc.description.abstractThe developing brain is the most susceptible target for methylmercury (MeHg) toxicity. Typical features of developmental MeHg neurotoxicity include the delayed onset of symptoms and the persistency of dysfunction. One of the factors which may modulate MeHg neurotoxicity is co-exposure to other neurotoxic pollutant, e.g. polychlorinated biphenyls (PCBs) from the same dietary sources. Because PCBs themselves can induce subtle neurodevelopmental deficiencies, recent epidemiological and research studies have focused on the potential hazard resulting from mixtures of PCBs and MeHg. This work summarizes our experimental findings on several endpoints of the cholinergic and aminergic systems in the developing rat brain, following two distinct perinatal co-exposure protocols involving low to moderate doses of MeHg and PCB153 or PCB126. The neurochemical modifications induced by either agent, alone or combined, involved monoamineoxidase type-B activity, biogenic amine levels (e.g., serotonin and dopamine), total cholinergic muscarinic receptors (MRs) and M1, M2 and M3 subtypes. The effects were brain region-, age- and gender-dependent. Some early-onset changes (weaning) persisted until puberty, while other alterations became manifest only at the advanced time point, when the brain levels of Hg, PCB153, and PCB126 had declined. The results of the combined exposure ruled out synergistic interactions between MeHg and PCB153 or PCB126 on every neurochemical endpoint tested. This applied to all pups regardless of the (i) regimen of exposure, (ii) gender, (iii) age, and (iv) brain area. The co-treatment with either PCB153 or PCB126 sometimes masked MeHg-induced changes on selected neurochemical endpoints. Nevertheless, this cannot be viewed as a protective effect. The final health effect may be masked at early time-points, but may become manifest later during life time.en_GB
dc.description.sponsorshipJRC.I.5-Physical and chemical exposuresen_GB
dc.format.mediumPrinteden_GB
dc.languageENGen_GB
dc.publisherPARLAR SCIENTIFIC PUBLICATIONS (P S P)en_GB
dc.relation.ispartofseriesJRC45634en_GB
dc.titleStudy of Polychlorinated Biphenyls as Potential Modifiers of Developmental Neurotoxicity of Methylmercuryen_GB
dc.typeArticles in periodicals and booksen_GB
JRC Directorate:Institute for Health and Consumer Protection Historical Collection

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