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Behavioral, Morphological, and Biochemical Changes after In Ovo Exposure to Methylmercury in Chicks

Methylmercury (MeHg) is an environmental pollutant known to induce neurotoxicity in several animal species, including humans. However, studies focusing the effects of MeHg poisoning in chicks were based on phenomenological approaches and did not delve into the molecular mechanisms. The purpose of th...

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Published in:Toxicological sciences 2008-11, Vol.106 (1), p.180-185
Main Authors: Carvalho, Márcia C., Nazari, Evelise M., Farina, Marcelo, Muller, Yara M. R.
Format: Article
Language:English
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Summary:Methylmercury (MeHg) is an environmental pollutant known to induce neurotoxicity in several animal species, including humans. However, studies focusing the effects of MeHg poisoning in chicks were based on phenomenological approaches and did not delve into the molecular mechanisms. The purpose of this study was to evaluate the postnatal consequences of the in ovo exposure to MeHg on behavioral, morphological and biochemical parameters in chicks. At the fifth embryonic day (E5), Gallus domesticus eggs were submitted to a single injection of 0.1 μg MeHg/0.05 ml saline. After treatment, the eggs returned to the incubator until hatching (E21). From first to fifth postnatal days (PN 1–PN 5), the MeHg-treated chicks showed lower frequency of exploratory movements and a significantly higher frequency of wing and anomalous movements. Cerebellar glutathione (GSH) levels and the activities of the GSH-related enzymes GSH reductase and GSH peroxidase were significantly higher (70, 72, and 80%, respectively) in MeHg exposed chicks in comparison to controls. Mercury impregnation was densest in the granular layer, followed by the Purkinje and molecular layers of treated chicks. A significant reduction of the number of Purkinje cells, as well as a greater distance between these cells were observed in chicks of MeHg group. Our results disclose that the prehatching exposure to MeHg induced motor impairments, which were correlated to histological damage and alterations on the cerebellar GSH system's development from PN 1 to PN 5.
ISSN:1096-6080
1096-0929
DOI:10.1093/toxsci/kfn158