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Polybrominated Diphenyl Ether (PBDE)...

Noyes, Pamela Diane.

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Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Accumulation, Metabolism and Disrupted Thyroid Regulation in Early and Adult Life Stages of Fish.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Accumulation, Metabolism and Disrupted Thyroid Regulation in Early and Adult Life Stages of Fish./
作者:	Noyes, Pamela Diane.
面頁冊數:	342 p.
附註:	Source: Dissertation Abstracts International, Volume: 74-07(E), Section: B.
Contained By:	Dissertation Abstracts International74-07B(E).
標題:	Environmental Sciences. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3556767
ISBN:	9781267991003

Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Accumulation, Metabolism and Disrupted Thyroid Regulation in Early and Adult Life Stages of Fish.
Noyes, Pamela Diane.

Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Accumulation, Metabolism and Disrupted Thyroid Regulation in Early and Adult Life Stages of Fish. - 342 p.

Source: Dissertation Abstracts International, Volume: 74-07(E), Section: B.

Thesis (Ph.D.)--Duke University, 2013.

Polybrominated diphenyl ethers (PBDEs) are a class of brominated flame retardant chemicals that are added to plastics, electronic components, furniture foam, and textiles to reduce their combustibility. The overall objective of this thesis research was to answer questions concerning how fish, as important indicators of overall environmental health, are metabolizing PBDEs and whether and how PBDEs are disrupting thyroid hormone regulation. The central hypothesis was that PBDE metabolism in fish is mediated by iodothyronine deiodinase (dio) enzymes, which are responsible for activating and inactivating thyroid hormones, and that PBDE exposures are causing thyroid system dysfunction across fish life stages.

ISBN: 9781267991003Subjects--Topical Terms:

676987
Environmental Sciences.

Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Accumulation, Metabolism and Disrupted Thyroid Regulation in Early and Adult Life Stages of Fish.
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245 1 0 $a Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Accumulation, Metabolism and Disrupted Thyroid Regulation in Early and Adult Life Stages of Fish.
300 $a 342 p.
500 $a Source: Dissertation Abstracts International, Volume: 74-07(E), Section: B.
500 $a Adviser: Heather M. Stapleton.
502 $a Thesis (Ph.D.)--Duke University, 2013.
520 $a Polybrominated diphenyl ethers (PBDEs) are a class of brominated flame retardant chemicals that are added to plastics, electronic components, furniture foam, and textiles to reduce their combustibility. The overall objective of this thesis research was to answer questions concerning how fish, as important indicators of overall environmental health, are metabolizing PBDEs and whether and how PBDEs are disrupting thyroid hormone regulation. The central hypothesis was that PBDE metabolism in fish is mediated by iodothyronine deiodinase (dio) enzymes, which are responsible for activating and inactivating thyroid hormones, and that PBDE exposures are causing thyroid system dysfunction across fish life stages.
520 $a Under the first research aim, in vitro experiments conducted in liver tissues isolated from common carp (Cyprinus carpio) suggested a role for dio enzymes in catalyzing the reductive debromination of PBDEs. Carp liver microsomes efficiently debrominated BDE-99 to BDE-47, and enzymes catalyzing this reaction were associated predominantly with the endoplasmic reticulum (i.e., microsomal fraction) where dio enzymes are located. Competitive substrate experiments in carp liver microsomes also demonstrated that rates of BDE-99 debromination to BDE-47 were significantly inhibited upon challenges with 3,3',5'-triiodothyronine (rT3) and thyroxine (T4). This finding supported the hypothesis that enzymes involved in the metabolism of PBDEs may have high affinities for thyroid hormones. Indeed, experiments to determine apparent enzymatic kinetics (apparent Vmax and K m values) of BDE-99 hepatic metabolism suggested that enzymes responsible for the catalytic activity appeared to have a higher affinity for native thyroid hormone than BDE-99.
520 $a The second and third research aims were focused on evaluating BDE-209 accumulation, metabolism, and thyroid toxicity in juvenile and adult life stages of fish using the fathead minnow (Pimephales promelas) as a model. BDE-209 bioaccumulated and was debrominated to several reductive metabolites ranging from penta- to octaBDEs in both juvenile and adult fish exposed to BDE-209. In addition, thyroid hormone regulation in juvenile and adult male fathead minnows was severely disrupted by BDE-209 at low, environmentally relevant exposures. In juvenile minnows, the activity of dio enzymes (T4-outer ring deiodination; T4-ORD and T4-inner ring deiodination; T4-IRD) declined by &sim;74% upon oral doses of 9.8 +/- 0.2 microg/g wet weight (ww) food at 3% body weight (bw)/day for 28 days, compared to controls. Declines in dio activity were accompanied by thyroid follicle hypertrophy indicative of over-stimulation and injury. In addition to thyroid disruption, a distinctive liver phenotype characterized by vacuolated hepatocyte nuclei was measured in &sim;48% of hepatocytes from treated fish that was not observed in controls.
520 $a Under the third research aim, adult male fathead minnows received dietary treatments of BDE-209 at a low dose (95.3 +/- 0.41 ng/g-food at 3% bw/day) and a high dose (10.1 +/- 0.10 microg/g-food at 3% bw/day) for 28 days followed by a 14-day depuration period to evaluate recovery. Compared to negative controls, adult male fish exposed orally to BDE-209 at the low dose tested for 28 days experienced a 53% and 46% decline in circulating total T4 and T3, respectively, while fish at the high BDE-209 dose tested had total T4 and T3 deficits of 59% and 62%, respectively. Depressed levels of plasma thyroid hormones were accompanied by a 45-50% decline in the rate of T4-ORD in brains of all treatments by day 14 of the exposure. The decreased T4-ORD continued in the brain at day 28 with a &sim;65% decline measured at both BDE-209 doses. BDE-209 exposures also caused transient, tissue-specific upregulations of relative mRNA transcripts encoding dio enzymes (dio1, dio2), thyroid hormone receptors (TRalpha, TRbeta), and thyroid hormone transporters (MCT8, OATP1c1) in the brain and liver in patterns that varied with time and dose, possibly as a compensatory response to hypothyroidism. In addition, thyroid perturbations at the low dose tested generally were equal to those measured at the high dose tested, suggesting non-linear relationships between PBDE exposures and thyroid dysfunction in adult fish. Thus, mechanisms for BDE-209 induced disruption of thyroid regulation can be proposed in adult male minnows that involve altered patterns of thyroid hormone signaling at several important steps in their transport and activation. (Abstract shortened by UMI.).
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