The promoter of the human sodium/iodide symporter responds to certain phthalate plasticisers

Breous, Ekaterina; Wenzel, Achim; Loos, U.

doi:10.1016/j.mce.2005.06.009

Cited by 93 publications

(55 citation statements)

References 23 publications

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“…This finding may contribute to thyroid hyperfunction. Certain phthalate plasticizers also increased the activity of NIS and enhanced NIS mRNA expression (Breous et al, 2005).…”

Section: Discussionmentioning

confidence: 94%

Waterborne exposure to PFOS causes disruption of the hypothalamus–pituitary–thyroid axis in zebrafish larvae

et al. 2009

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“…This finding may contribute to thyroid hyperfunction. Certain phthalate plasticizers also increased the activity of NIS and enhanced NIS mRNA expression (Breous et al, 2005).…”

Section: Discussionmentioning

confidence: 94%

Waterborne exposure to PFOS causes disruption of the hypothalamus–pituitary–thyroid axis in zebrafish larvae

et al. 2009

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“…2). In contrast, phthalates such as DIDP, butyl benzyl phthalate (BBP) and DnOP increased the activity of the NIS and enhanced NIS mRNA expression (115). TPO activity was inhibited in vitro by NP (61).…”

Section: Mechanisms Of Actionmentioning

confidence: 99%

Environmental chemicals and thyroid function

Boas¹,

Feldt‐Rasmussen

Skakkebæk³

et al. 2006

eur j endocrinol

458

290

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There is growing evidence that environmental chemicals can disrupt endocrine systems. Most evidence originates from studies on reproductive organs. However, there is also suspicion that thyroid homeostasis may be disrupted. Several groups of chemicals have potential for thyroid disruption. There is substantial evidence that polychlorinated biphenyls, dioxins and furans cause hypothyroidism in exposed animals and that environmentally occurring doses affect human thyroid homeostasis. Similarly, flame retardants reduce peripheral thyroid hormone (TH) levels in rodents, but human studies are scarce. Studies also indicate thyroid-disruptive properties of phthalates, but the effect of certain phthalates seems to be stimulative on TH production, contrary to most other groups of chemicals. Thyroid disruption may be caused by a variety of mechanisms, as different chemicals interfere with the hypothalamic -pituitary -thyroid axis at different levels. Mechanisms of action may involve the sodium-iodide symporter, thyroid peroxidase enzyme, receptors for THs or TSH, transport proteins or cellular uptake mechanisms. The peripheral metabolism of the THs can be affected through effects on iodothyronine deiodinases or hepatic enzymes. Even small changes in thyroid homeostasis may adversely affect human health, and especially fetal neurological development may be vulnerable. It is therefore urgent to clarify whether the animal data showing effects of chemicals on thyroid function can be extended to humans. European Journal of Endocrinology 154 599-611

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“…DEHP significantly enhanced iodide uptake when concentrations in the magnitude between 10 −4 and 10 −3 M were applied . Breous et al (2005) suggested that the increase in iodide uptake in a rat thyroid cell line (PC C13 cells) was the consequence of NIS transcriptional activation by DEHP. Another potential mechanism mentioned is associated with transthyretin (TTR).…”

Section: Introductionmentioning

confidence: 99%

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

136

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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.

show abstract

The promoter of the human sodium/iodide symporter responds to certain phthalate plasticisers

Cited by 93 publications

References 23 publications

Waterborne exposure to PFOS causes disruption of the hypothalamus–pituitary–thyroid axis in zebrafish larvae

Waterborne exposure to PFOS causes disruption of the hypothalamus–pituitary–thyroid axis in zebrafish larvae

Environmental chemicals and thyroid function

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

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