Subchronic effects of 2,3,7,8-TCDD or PCBs on thyroid hormone metabolism: use in risk assessment

Birgelen, A.P.J.M. van; Smit, Elize; Kampen, Ingo; Groeneveld, C.N.; Fase, K.M.; Kolk, J. van der; Poiger, H.; Berg, Martin van den; Koeman, J.H.; Brouwer, Abraham

doi:10.1016/0926-6917(95)90021-7

Cited by 111 publications

(56 citation statements)

References 41 publications

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“…As a possible explanation for a chemical-induced decrease in serum thyroid hormones, a hepatic T 4 -UDP-GT-dependent mechanism is generally considered, because T 4 -UDP-GT inducers, including PCB, phenobarbital, 3-methylcholanthrene, pregnenolone-16␣-carbonitrile, and clobazam, show strong activities for decreasing the level of serum total thyroid hormones, including T 4 and T 3 (Barter and Klaassen, 1994;Van Birgelen et al, 1995;Miyawaki et al, 2003). However, among the experimental animals treated with a T 4 -UDP-GT inducer, the difference in magnitude of decrease in the level of serum total T 4 is not necessarily correlated with that of hepatic T 4 -UDP-GT activity (Craft et al, 2002;Hood et al, 2003;Kato et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Most polychlorinated biphenyls (PCBs) are known to decrease the level of serum thyroid hormone and to increase the activity of hepatic drug-metabolizing enzymes in rats (Van Birgelen et al, 1995;Craft et al, 2002). As possible mechanisms for the PCBinduced decrease in the level of serum thyroid hormone, enhancement of thyroid hormone metabolism by PCB and displacement of the hormone from serum transport proteins, including transthyretin (TTR), by PCB and its ring-hydroxylated metabolites are considered Klaassen, 1992a, 1994;Brouwer et al, 1998).…”

mentioning

confidence: 99%

“…As possible mechanisms for the PCBinduced decrease in the level of serum thyroid hormone, enhancement of thyroid hormone metabolism by PCB and displacement of the hormone from serum transport proteins, including transthyretin (TTR), by PCB and its ring-hydroxylated metabolites are considered Klaassen, 1992a, 1994;Brouwer et al, 1998). In particular, the decrease in the level of serum thyroxine (T 4 ) by 3,3Ј,4,4Ј,5-pentachlorobiphenyl, Aroclor 1254, and 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats is believed to occur mainly through induction of the UDP-glucuronosyltransferases (UDP-GTs), especially UGT1A subfamily enzymes, responsible for glucuronidation of T 4 (Barter and Klaassen, 1994;Van Birgelen et al, 1995).…”

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confidence: 99%

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A Novel Mechanism for Polychlorinated Biphenyl-Induced Decrease in Serum Thyroxine Level in Rats

Kato

Ikushiro²,

Takiguchi³

et al. 2007

Drug Metabolism and Disposition

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ABSTRACT:We have previously suggested that the decrease in the levels of serum total thyroxine (T 4 ) and free T 4 by a single administration to rats of Kanechlor-500 (KC500) at a dose of 100 mg/kg is not necessarily dependent on the increase in hepatic T 4 -UDP-glucuronosyltransferase (UDP-GT). In the present study, we determined whether or not a consecutive treatment with KC500 at a relatively low dose (10 mg/kg i.p., once daily for 10 days) results in a decrease in the level of serum total T 4 and further investigated an exact mechanism for the KC500-induced decrease in the T 4 . At 4 days after final treatment with KC500, the serum total T 4 and free T 4 levels were markedly decreased in both Wistar and UGT1A-deficient Wistar (Gunn) rats, whereas significant increases in hepatic T 4 -UDP-GT activity were observed in

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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A Novel Mechanism for Polychlorinated Biphenyl-Induced Decrease in Serum Thyroxine Level in Rats

Kato

Ikushiro²,

Takiguchi³

et al. 2007

Drug Metabolism and Disposition

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“…A number of OHPCBs identified in human serum exhibited antiestrogenic activity in the rat uterine estrogen-binding assay and in the MCF-7 cell proliferation assay (9). OH-PCBs bound to the estrogen receptor and transactivated the estrogen receptor to DNA binding and altered gene expression in in vitro reporter gene assays (9,10 (17). PCB mixtures are also capable of inducing T4 glucuronidation (18)(19)(20)(21).…”

Section: Estrogen Receptor-mediated Effectsmentioning

confidence: 99%

Characterization of Potential Endocrine-Related Health Effects at Low-Dose Levels of Exposure to PCBs

Brouwer¹,

Longnecker²,

Birnbaum³

et al. 1999

Environmental Health Perspectives

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This article addresses issues related to the characterization of endocrine-related health effects resulting from low-level exposures to polychlorinated biphenyls (PCBs). It is not intended to be a comprehensive review of the literature but reflects workshop discussions. "The Characterizing the Effects of Endocrine Disruptors on Human Health at Environmental Exposure Levels," workshop provided a forum to discuss the methods and data needed to improve risk assessments of endocrine disruptors. This article contains an overview of endocrine-related (estrogen and thyroid system) interactions and other low-dose effects of PCBs. The data set on endocrine effects includes results obtained from mechanistic methods/ and models (receptor based, metabolism based, and transport protein based), as well as from in vivo models, including studies with experimental animals and wildlife species. Other low-dose effects induced by PCBs, such as neurodevelopmental and reproductive effects and endocrine-sensitive tumors, have been evaluated with respect to a possible causative linkage with PCB-induced alterations in endocrine systems. In addition, studies of low-dose exposure and effects in human populations are presented and critically evaluated. A list of conclusions and recommendations is included.

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“…TCDD and related compounds have been demonstrated to alter cell growth and differentiation, and to affect homeostasis and hormone balance by modulating the induction of enzymes, growth factors and hormones as well as their cognate receptors (DeVito & Birnbaum 1995). In addition, these xenobiotic compounds can act in an estrogenic or antiestrogenic manner (Safe & Krishnan 1995), alter the levels of thyroxin (Van Birgelen et al 1995) and several growth factors -including their cognate receptors (Abbott & Birnbaum 1990, Dohr et al 1994) -or modulate the expression of glucocorticoids (Abbott 1995).…”

Section: Introductionmentioning

confidence: 99%

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Pocar

Fischer²,

Klonisch³

et al. 2005

Reproduction

168

126

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The dioxin/aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor responsive to both natural and man-made environmental compounds. AhR and its nuclear partner ARNT are expressed in the female reproductive tract in a variety of species and several indications suggest that the AhR might play a pivotal role in the physiology of reproduction. Furthermore, it appears to be the mediator of most, if not all, the adverse effects on reproduction of a group of highly potent environmental pollutants collectively called aryl hydrocarbons (AHs), including the highly toxic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Although a large body of recent literature has implicated AhR in multiple signal transduction pathways, the mechanisms of action resulting in a wide spectrum of effects on female reproduction are largely unknown. Here we summarize the major types of molecular cross-talks that have been identified for the AhR and linked cell signaling pathways and that are relevant for the understanding of the role of this transcription factor in female reproduction.

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Subchronic effects of 2,3,7,8-TCDD or PCBs on thyroid hormone metabolism: use in risk assessment

Cited by 111 publications

References 41 publications

A Novel Mechanism for Polychlorinated Biphenyl-Induced Decrease in Serum Thyroxine Level in Rats

A Novel Mechanism for Polychlorinated Biphenyl-Induced Decrease in Serum Thyroxine Level in Rats

Characterization of Potential Endocrine-Related Health Effects at Low-Dose Levels of Exposure to PCBs

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

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