Abstract
Polybrominated diphenyl ethers (PBDEs) are a class of brominated flame retardants that are recognized as global environmental contaminants and a potential health risk. They have been shown to elicit neurodevelopmental toxicity through disruption of the cholinergic neurotransmitter system in rodent models, but the effects of environmentally relevant exposures in wildlife species are unknown. The objective of this study was to assess the effects of the commercial pentabrominated diphenyl ether mixture DE-71 on cholinergic parameters in ranch mink (Mustela vison) following dietary exposure of adult females and in utero, lactational, and dietary exposure of their offspring. Adult females were fed diets containing 0, 0.1, 0.5, or 2.5 μg DE-71/g feed from four weeks prior to breeding through weaning of their kits at six weeks of age. A portion of the weaned kits were maintained on their respective diets through 27 weeks of age. Cholinergic parameters, including muscarinic acetylcholine receptor (mAChR) and nicotinic acetylcholine receptor (nAChR) binding, cholinesterase (ChE) activity, and acetylcholine (ACh) concentration, were assayed in the cerebral cortex, and ChE activity was measured in the plasma. In the cerebral cortex, results indicated a significant exposure-dependent increase in PBDE concentrations, but no significant effects of DE-71 on cholinergic parameters. There was a threefold increase in ChE activity in the plasma of adult females in the 2.5 μg DE-71/g feed group, but was likely due to effects on liver function. This study demonstrated that environmentally relevant exposures to DE-71 did not affect key parameters of the cholinergic neurotransmitter system in the brain of ranch mink. © 2007 Oxford University Press.
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Bull, K., Basu, N., Zhang, S., Martin, J. W., Bursian, S., Martin, P., & Chan, L. H. M. (2007). Dietary and in utero exposure to a pentabrominated diphenyl ether mixture did not affect cholinergic parameters in the cerebral cortex of ranch mink (Mustela vison). Toxicological Sciences, 96(1), 115–122. https://doi.org/10.1093/toxsci/kfl179
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