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ToxSci Advance Access published online on November 2, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfm271
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© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Co-exposure of neonatal mice to a flame retardant PBDE 99 (2,2',4,4',5-pentabromodiphenyl ether) and methylmercury enhances developmental neurotoxic defects

Celia Fischer, Anders Fredriksson and Per Eriksson

Department of Environmental Toxicology, Uppsala University, Norbyvägen 18A, S-752 36 Uppsala, Sweden

Correspondence to: Per Eriksson, Department of Environmental Toxicology, Evolutionary Biology Centre, Uppsala University, Norbyvägen 18A, S-752 36 Uppsala, Sweden, Tel: +46 18 4712623, FAX: +46 18 518843, E-mail: per.eriksson{at}ebc.uu.se

Received August 17, 2007; revision received October 5, 2007; accepted October 7, 2007


  Abstract

Epidemiological studies indicate that exposure to environmental pollutants during early human development can have deleterious effects on cognitive development. The interaction between environmental pollutants is suggested as one reason for the observed defective neurological development in children from the Faeroe Islands as compared to children from the Seychelles. We have previously seen in mice that polychlorinated biphenyls (PCB) can interact together with MeHg, as well as PCB together with polybrominated diphenyl ether (PBDE 99) to exacerbate developmental neurotoxic effects when present during a critical period of neonatal brain development. PBDEs are a new class of global environmental contaminants.

The present study shows that neonatal co-exposure to PBDE 99 (0.8 mg/kg body weight) and MeHg (0.4 or 4.0 mg/kg body weight) can exacerbate developmental neurotoxic effects. These effects are manifested as disrupted spontaneous behavior, reduced habituation, and impaired learning/memory abilities. This is seen in the low dose range, where the sole compounds do no give rise to developmental neurotoxic effects. The effects seen are more than just additive. Furthermore, a significant effect of interaction was seen on the cholinergic nicotinic receptors in the cerebral cortex and hippocampus. This suggests that a mechanism for the observed cognitive defects is via the cholinergic system. Furthermore PBDE can interact with MeHg causing developmental neurotoxic effects similar to those we previously have observed between PCB 153 + MeHg and PCB 52 + PBDE 99. This is of vital importance, as the levels of PBDEs are increasing in mother's milk and in the environment generally.

Key Words: PBDE; methyl mercury; behavior; cholinergic receptors; neonatal; neurotoxicity.


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