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Polybrominated diphenyl ethers, a group of brominated flame retardants, can interact with polychlorinated biphenyls in enhancing developmental neurobehavioral defects
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
2006 (English)In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 94, no 2, 302-309 p.Article in journal (Refereed) Published
Abstract [en]

The present study shows that polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) can interact and enhance developmental neurobehavioral defects when the exposure occurs during a critical stage of neonatal brain development. PBDEs are used in large quantities as flame-retardant additives in polymers, especially in the manufacture of a great variety of electrical appliances, and textiles. In contrast to the well-known persistent compounds PCBs and DDT, the PBDEs have been found to increase in the environment and in human mother's milk. We have previously shown that low-dose exposure to environmental toxic agents such as PCB can cause developmental neurotoxic effects when present during a critical stage of neonatal brain development. Epidemiological studies indicate the adverse neurobehavioral impact of PCBs. Recently, we reported that neonatal exposure to PBDEs causes developmental neurotoxic effects. In the present study, 10-day-old Naval Medical Research Institute male mice were given one single oral dose of PCB 52 (1.4 mu mol/kg body weight [bw]) + PBDE 99 (1.4 mu mol), PCB 52 (1.4 mu mol or 14 mu mol), or PBDE 99 (1.4 mu mol or 14 mu mol). Controls received a vehicle (20% fat emulsion). Animals exposed to the combined dose of PCB 52 (1.4 mu mol) + PBDE 99 (1.4 mu mol) and the high dose of PCB 52 (14 mu mol) or PBDE 99 (14 mu mol) showed significantly impaired spontaneous motor behavior and habituation capability at the age of 4 and 6 months. The neurobehavioral defects were also seen to worsen with age in mice neonatally exposed to PCB 52 + PBDE 99.

Place, publisher, year, edition, pages
2006. Vol. 94, no 2, 302-309 p.
Keyword [en]
PBDE, PCB, brominated flame retardants, behavior, habituation, neonatal, neurotoxicity
National Category
Biological Sciences
Identifiers
URN: urn:nbn:se:uu:diva-96658DOI: 10.1093/toxsci/kfl109ISI: 000242273400008PubMedID: 16980691OAI: oai:DiVA.org:uu-96658DiVA: diva2:171306
Available from: 2008-01-18 Created: 2008-01-18 Last updated: 2011-05-06Bibliographically approved
In thesis
1. Developmental Neurotoxicity in Mice Neonatally Co-exposed to Environmental Agents: PCB, PBDE, Methyl Mercury and Ionized Radiation - Interactions and Effects
Open this publication in new window or tab >>Developmental Neurotoxicity in Mice Neonatally Co-exposed to Environmental Agents: PCB, PBDE, Methyl Mercury and Ionized Radiation - Interactions and Effects
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

This thesis investigates the neurotoxic effects in mice neonatally co-exposed to different toxic environmental agents during a defined critical period of the brains's rapid growth and development.

Environmental toxic agents are incorporated in our environment. The agents investigated in this thesis are ortho-substituted polychlorinated biphenyls (PCBs 52, and 153), co-planar PCB (PCB 126), polybrominated diphenyl ether (PBDE 99), methyl mercury (MeHg), and γ-radiation. Several epidemiological studies show that human exposure to environmental agents during early development can affect childhood cognitive development.

The brain growth spurt (BGS) is defined by rapid growth and development of the immature brain. For rodents (rats and mice) the BGS is postnatal spanning the first 3-4 weeks after birth. For humans this period begins during the third trimester of pregnancy and continues throughout the first two years of life. Several studies have shown that the BGS period of the brain's development renders the brain vunerable and susceptible to insults caused by environmental agents.

The combinations of environmental agents used in this thesis were: PCB 52 + PBDE 99, PCB 153 + MeHg, PCB 126 + MeHg, PBDE 99 + MeHg, and γ-radiation + MeHg. The studies presented in this thesis show that co-exposure to low doses of environmental agents lead to interaction effects. These effects of interaction include defective spontaneous behavior, diminished habituation capabilities and hyperactive condition, decreased learning and memory abilities, and reduction in the nicotinic cholinergic receptor densities.

Traditionally environmental agents are evaluated one at a time to investigate their effects of toxicity. This thesis indicates that the effects of interaction caused by co-exposure were often seen at doses where exposure to the individual environmental agent alone did not cause any effect. The observed effect of co-exposure were often as pronounced as a dose up to ten times the individual environmental agent alone.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2008. 76 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology, ISSN 1651-6214 ; 387
Keyword
Biology, PCB, PBDE, MeHg, ionized radiation, neonatal, development, neurotoxicity, behavior, cholinergic system, Biologi
Identifiers
urn:nbn:se:uu:diva-8416 (URN)978-91-554-7071-5 (ISBN)
Public defence
2008-02-09, Lindahlsalen, EBC, Norbyvägen 18A, Uppsala, 10:00 (English)
Opponent
Supervisors
Available from: 2008-01-18 Created: 2008-01-18 Last updated: 2009-04-02Bibliographically approved

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Eriksson, PerFischer, CeliaFredriksson, Anders

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