Polychlorinated biphenyl effects on avian hepatic enzyme induction and thyroid function

Webb, Catherine M.; McNabb, F. M. Anne

doi:10.1016/j.ygcen.2007.09.010

Cited by 30 publications

(21 citation statements)

References 41 publications

(132 reference statements)

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“…Induced UDPGTs could accelerate the metabolism and excretion of THs. Moreover, studies suggested that liver weight is expected to increase in many species due to hepatic enzyme induction (Webb and McNabb 2008). Our current study also observed that liver weight of DEHP-exposed rats was significantly elevated.…”

Section: Discussionsupporting

confidence: 81%

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats

Liu

Zhao

et al. 2015

Environ Sci Pollut Res

130

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Di-(2-ethylhexyl) phthalate (DEHP) is used extensively in many personal care and consumer products, resulting in widespread nonoccupational human exposure through multiple routes and media. Limited studies suggest that exposure to DEHP may be associated with altered thyroid function, but detailed mechanisms are unclear. In order to elucidate potential mechanisms by which DEHP disturbs thyroid hormone homeostasis, Sprague-Dawley (SD) rats were dosed with DEHP by gavage at 0, 250, 500, and 750 mg/kg/day for 30 days and sacrificed within 24 h after the last dose. Gene expressions of thyroid hormone receptors, deiodinases, transthyretin, and hepatic enzymes were measured by RT-PCR; protein levels of transthyretin were also analyzed by Western blot. Results showed that DEHP caused histological changes in the thyroid and follicular epithelial cell hypertrophy and hyperplasia were observed. DEHP significantly reduced thyroid hormones (T3, T4) and thyrotropin releasing hormone (TRH) levels, whereas thyroid stimulating hormone (TSH) was not affected. After exposure to DEHP, biosynthesis of thyroid hormones was suppressed, and sodium iodide symporter (NIS) and thyroid peroxidase (TPO) levels were significantly reduced. Additionally, levels of deiodinases and transthyretin were also affected. TSH receptor (TSHr) level was downregulated, while TRH receptor (TRHr) level was upregulated. Metabolism of thyroid hormones was accelerated due to elevated gene expression of hepatic enzymes (UDPGTs and CYP2B1) by DEHP. Taken together, observed findings indicate that DEHP could reduce thyroid hormones through influencing biosynthesis, biotransformation, biotransport, receptor levels, and metabolism of thyroid hormones.

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Section: Discussionsupporting

confidence: 81%

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats

Liu

Zhao

et al. 2015

Environ Sci Pollut Res

130

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“…Numerous studies have demonstrated that TCDD and PCBs change thyroxine (T 4 ) and triiodothyronine (T 3 ) concentrations in the blood of rodents (Craft et al, 2002;Desaulniers et al, 1999;Khan et al, 2002) and humans (Nagayama et al, 1998;Schell et al, 2004). Three possible ways of this particular disruption have been proposed: (1) direct inhibition of the pituitary or thyroid gland (Webb and McNabb, 2008), (2) displacement of T 4 from thyroid hormone binding proteins and the consequent release of free T 4 , resulting in enhanced metabolism and excretion (Chauhan et al, 2000;Pearce and Braverman, 2009), (3) induction of hepatic uridine diphosphate glucuronosyl-transferases (UDPGTs) activity mediated by AhR, and subsequent enhanced exertion of T 4 -glucuronide in bile (Hood et al, 2003;Kato et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…In birds, the effect of dioxins and PCBs on thyroid function has been also investigated (McNabb and Fox, 2003;Piskač et al, 1990;Ruprich and Piskač, 1990;Van den Berg et al, 1998), indicating that thyroid function in birds appears to be less susceptible to dioxin and PCBs than in mammals (Webb and McNabb, 2008). Surprisingly, in the available literature there are no comparative studies concerning effects of dioxin, dioxin-like coplanar and non-coplanar PCBs on thyroid hormone synthesis in laying chickens.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the in vitro effects of TCDD, PCB 126 and PCB 153 on thyroid-restricted gene expression and thyroid hormone secretion by the chicken thyroid gland

Katarzyńska

Hrabia

Kowalik

et al. 2015

Environmental Toxicology and Pharmacology

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“…This finding indicates that the redistribution of HOCs to the liver induces hepatic UDPGT mRNA expression. A PCB-mediated induction of hepatic UDPGT has also been observed in Japanese quail (Coturnix japonica) [47].…”

Section: Effect Of Fasting On Toxicokinetics Of Hocs In Herring Gullsmentioning

confidence: 85%

Effect of reduced food intake on toxicokinetics of halogenated organic contaminants in herring gull (Larus argentatus) chicks

Routti

Helgason

Arukwe

et al. 2012

Enviro Toxic and Chemistry

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Abstract-The aim of the present study was to investigate how contaminant exposure and reduced food intake affect tissue distribution and biotransformation of halogenated organic contaminants (HOCs) in Arctic seabirds using herring gull (Larus argentatus) as a model species. Herring gull chicks were exposed for 44 d to cod liver oil containing a typical mixture of contaminants. Following exposure, food intake was reduced for a one-week period in a subgroup of the chicks. Polyclorinated biphenyls, organochlorine pesticides, and brominated flame retardants, as well as a wide range of hydroxy, methyl sulfone, and methoxy compounds were measured in liver, brain, and plasma samples. Additionally, phase I biotransformation enzyme activities and phase I and II messenger ribonucleic acid (mRNA) expression were investigated in the liver, brain, or both. Both contaminant exposure and reduced food intake had an increasing effect on the concentrations of HOCs and their metabolites. The HOC exposure and reduced food intake also led to increased 7-ethoxyresorufin-O-deethylation (EROD) activity, whereas mRNA expression of the biotransformation enzymes increased only following the reduced food intake. Tissue distribution of HOCs and their metabolites was not affected by either contaminant exposure or reduced food intake. In conclusion, the results indicate that biotransformation capacity and formation of HOC metabolites increase during reduced food intake. This finding supports the hypothesis that reduced food intake increases the susceptibility of Arctic animals to the effects of lipophilic HOCs. Environ. Toxicol. Chem. 2013;32:156-164. # 2012 SETAC

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Polychlorinated biphenyl effects on avian hepatic enzyme induction and thyroid function

Abstract: Polychlorinated biphenyls (PCBs) decrease thyroid function in rats and mice by

Cited by 30 publications

References 41 publications

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats

Comparison of the in vitro effects of TCDD, PCB 126 and PCB 153 on thyroid-restricted gene expression and thyroid hormone secretion by the chicken thyroid gland

Effect of reduced food intake on toxicokinetics of halogenated organic contaminants in herring gull (Larus argentatus) chicks

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