Polychlorinated biphenyl effects on avian hepatic enzyme induction and thyroid function

Department of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061-0406, USA.
General and Comparative Endocrinology (Impact Factor: 2.47). 03/2008; 155(3):650-7. DOI: 10.1016/j.ygcen.2007.09.010
Source: PubMed


Polychlorinated biphenyls (PCBs) decrease thyroid function in laboratory rodents by inducing activity of a liver enzyme, uridine diphosphate-glucuronosyltransferase (UDP-GT), thereby increasing thyroxine (T4) clearance. This loss of T4 can lead to hypothyroidism. In this study, an assay was validated for measuring UDP-GT activity toward T4 in Japanese quail. UDP-GT induction by Aroclor 1254 was evaluated in quail, and responses of quail and mice were compared. In Experiment 1, Japanese quail and Balb/c mice were dosed orally with vehicle or Aroclor 1254 (250 or 500mg/kg) and sacrificed 5days later. In Experiment 2, Japanese quail were dosed orally with vehicle or Aroclor 1254 (500mg/kg) and sacrificed 5 or 21days later. UDP-GT capacity (pmol T4 glucuronidated by the liver/minper g body weight) increased with PCB exposure with all doses and exposure times in both species. Plasma T4 tended to decrease (not significant) with both PCB doses and exposure times in quail and was significantly decreased with both doses in mice. Quail did not become hypothyroid at either dose or exposure time. In contrast, mice did become hypothyroid after a 5-day exposure. It is unclear how PCBs affect the hypothalamic-pituitary-thyroid (HPT) axis in quail, but activation of the HPT axis appears to be inhibited in mice. We believe this is the first demonstration of a T4-specific, avian UDP-GT response to PCBs. However, this avian response was less than that in mice with equivalent doses of PCBs. Thus, thyroid function in birds appears to be less vulnerable to PCBs than in mammals.

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    • ", 2002 ; Skarman et al . , 2005 ) and in adult Japanese quails orally dosed with a PCB commercial mixture ( Aroclor 1254 ) during 5 and 21 days ( Webb and McNabb , 2008 ) . "
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    ABSTRACT: A number of studies have reported altered circulating thyroid hormone levels in birds exposed either in controlled settings or in their natural habitat to ubiquitous organohalogen compounds including organochlorines (OCs) and polybrominated diphenyl ether (PBDE) flame retardants. However, limited attention has been paid to underlying homeostatic mechanisms in wild birds such as changes in the expression of genes in the hypothalamic-pituitary-thyroid (HPT) axis. The objective of the present study was to investigate the relationships between hepatic concentrations of major organohalogens (PBDEs and OCs), and circulating thyroid hormone (free and total thyroxine (T4) and triiodothyronine (T3)) levels and transcription of 14 thyroid-related genes in three tissues (thyroid, brain, and liver) of an urban-adapted bird exposed to high organohalogen concentrations in the Montreal area (QC, Canada), the ring-billed gull (Larus delawarensis). Positive correlations were found between liver concentrations of several polychlorinated biphenyls (PCBs), PBDEs as well as chlordanes and total plasma T4 levels. Hepatic concentrations of several PBDEs were negatively correlated with mRNA levels of deiodinase type 3, thyroid peroxidase, and thyroid hormone receptor β (TRβ) in the thyroid gland. Liver PCB (deca-CB) correlated positively with mRNA levels of sodium-iodide symporter and TRα. In brain, concentrations of most PBDEs were positively correlated with mRNA levels of organic anion transporter protein 1C1 and transthyretin, while PCBs positively correlated with expression of TRα and TRβ as well as deiodinase type 2. These multiple correlative linkages suggest that organohalogens operate through several mechanisms (direct or compensatory) involving gene transcription, thus potentially perturbing the HPT axis of this highly organohalogen-contaminated ring-billed gull population.
    Full-text · Article · Mar 2016 · Science of The Total Environment
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    • "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. "
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    ABSTRACT: The aim of this study was to compare the in vitro effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126; a coplanar PCB congener) and 2,2’4,4’,5,5’-hexachlorobiphenyl (PCB153; non-coplanar PCB) on mRNA expression of thyroid-restricted genes, i.e. sodium iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and thyroid hormone secretion from the thyroid gland of the laying chicken. Relative expression levels of NIS, TG and TPO genes and thyroxine (T4) and triiodothyronine (T3) secretion from the thyroidal explants were quantified by the real-time qPCR and RIA methods, respectively. In comparison with the control group, TCDD and PCB 126 significantly increased mRNA expression of TPO and TG genes. TCDD did not affect NIS mRNA levels, but PCB 126 decreased its expression. No effect of PCB 153 on the expression of these genes was observed. TCDD and PCB 126 significantly decreased T4 and T3 secretion. There was no significant effect of PCB 153 on these hormone secretions. In conclusion, the results obtained show that in comparison with non-coplanar PCB 153, TCDD and coplanar PCB 126 can directly affect thyroid hormone synthesis and secretion, and in consequence, they may disrupt the endocrine function of the thyroid gland of the laying chicken.
    Full-text · Article · Feb 2015 · Environmental Toxicology and Pharmacology
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