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Coplanar PCB-induced inflammation an...

Eske, Katryn Elizabeth.

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Coplanar PCB-induced inflammation and dietary interventions.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Coplanar PCB-induced inflammation and dietary interventions./
Author:	Eske, Katryn Elizabeth.
Description:	198 p.
Notes:	Source: Dissertation Abstracts International, Volume: 76-01(E), Section: B.
Contained By:	Dissertation Abstracts International76-01B(E).
Subject:	Health Sciences, Nutrition. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3583710
ISBN:	9781321192094

Coplanar PCB-induced inflammation and dietary interventions.
Eske, Katryn Elizabeth.

Coplanar PCB-induced inflammation and dietary interventions. - 198 p.

Source: Dissertation Abstracts International, Volume: 76-01(E), Section: B.

Thesis (Ph.D.)--University of Kentucky, 2013.

Diseases, such as cardiovascular disease (CVD), are linked to chronic low levels of inflammation. This inflamed state is the product of risk factors including exposure to environmental pollutants, such as polychlorinated biphenyls (PCBs), which are correlated with increased risk for CVD and diabetes. In response to this health risk, our research addresses the mechanisms by which coplanar PCBs elicit an inflammatory response and the mitigation of PCB-induced inflammation through dietary intervention using docosahexaenoic acid (DHA), an omega-3 lipid.

ISBN: 9781321192094Subjects--Topical Terms:

1017801
Health Sciences, Nutrition.

Coplanar PCB-induced inflammation and dietary interventions.
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020 $a 9781321192094
035 $a (MiAaPQ)AAI3583710
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040 $a MiAaPQ $c MiAaPQ
100 1 $a Eske, Katryn Elizabeth. $3 2105755
245 1 0 $a Coplanar PCB-induced inflammation and dietary interventions.
300 $a 198 p.
500 $a Source: Dissertation Abstracts International, Volume: 76-01(E), Section: B.
500 $a Adviser: Shuxia Wang.
502 $a Thesis (Ph.D.)--University of Kentucky, 2013.
520 $a Diseases, such as cardiovascular disease (CVD), are linked to chronic low levels of inflammation. This inflamed state is the product of risk factors including exposure to environmental pollutants, such as polychlorinated biphenyls (PCBs), which are correlated with increased risk for CVD and diabetes. In response to this health risk, our research addresses the mechanisms by which coplanar PCBs elicit an inflammatory response and the mitigation of PCB-induced inflammation through dietary intervention using docosahexaenoic acid (DHA), an omega-3 lipid.
520 $a Investigators from the University of Kentucky Engineering Department are developing remediation technologies that detoxify PCBs through dechlorination. We studied the cellular toxicity of coplanar PCB 77 remediation products in primary vascular endothelial cells. The dechlorination products elicited different toxicological responses, which were less than the parent compound and contributed to the overall inflammatory response. The presence of PCB 77 at any concentration was sufficient to promote an inflammatory response, which was attenuated with complete dechlorination.
520 $a PCB 77 is a good model for coplanar PCB-induced toxicity, but in environmental and human samples, coplanar PCB 126 is detected more frequently. Using different doses of PCB 126, we determined that acute exposure to 5 mumol PCB 126/kg mouse was sufficient to produce an inflammatory response without inducing a toxic wasting phenotype. PCB-induced inflammation was attenuated in vitro by DHA-derived neuroprostanes. Applying this information, we fed mice a DHA-enriched diet and exposed them to PCB 126. Liver and adipose lipid profiles confirm an increase in omega-3 fatty acid composition and DHA metabolites, and changes in gene expression indicate a heightened anti-oxidant response in the presence of PCB-induced inflammation. These data provide an overview of the in vivo response to a PCB-induced inflammation after DHA dietary feeding. We have demonstrated that PCB-induced endothelial dysfunction is propagated through lipid domains called caveolae. Caveolae are also signaling domains for toll-like receptor 4 (TLR4), and receptor for lipopolysaccharide (LPS). Similar to PCBs, TLR4 signaling is inhibited by DHA. We compared the caveolae-associated signaling response after exposure to coplanar PCB 126 or LPS. The domain localization of caveolae was altered by both PCB 126 and LPS. Our study determined that PCB 126-induced inflammation was not inhibited by a TLR4-specific inhibitor, but caveolae-based signaling was critical to both PCB 126- and LPS-induced inflammation.
520 $a Environmental pollutants, such as coplanar PCBs, are risk factors in the development of chronic diseases. Here we investigate possible signaling pathways associated with environmental toxicity and apply potential dietary interventions with omega-3 lipids.
520 $a KEYWORDS: Polychlorinated biphenyls (PCBs); endothelial cells; inflammation; docosahexaenoic acid (DHA); caveolae.
590 $a School code: 0102.
650 4 $a Health Sciences, Nutrition. $3 1017801
650 4 $a Health Sciences, Toxicology. $3 1017752
650 4 $a Environmental Health. $3 578282
690 $a 0570
690 $a 0383
690 $a 0470
710 2 $a University of Kentucky. $3 1017485
773 0 $t Dissertation Abstracts International $g 76-01B(E).
790 $a 0102
791 $a Ph.D.
792 $a 2013
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3583710