Functional Interactions of AHR with other Receptors

Brunnberg, Sara; Swedenborg, Elin; Gustafsson, Jan Åke

doi:10.1002/9781118140574.ch9

Cited by 6 publications

(6 citation statements)

References 138 publications

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“…It is worth pointing out that the focus of the present study was on the wasting syndrome, not on the mechanism(s) by which TCDD might directly alter hormonal status. Previous work has revealed that there is a wide spectrum of possible ways for TCDD to interfere with the endocrine balance, including enhanced potency of a positive regulator (ACTH [ 69 , 70 ]), induction of metabolism in the liver (thyroxin [ 71 ]) or extrahepatically (melatonin [ 72 ]), impaired synthesis (testosterone, corticosterone [ 73 , 74 ]), and induction of interactions between the AHR and hormone receptors (estrogen and androgen receptors [ 75 ]).…”

Section: Resultsmentioning

confidence: 99%

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

Lindén

Lensu

Pohjanvirta

2014

IJMS

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One of the hallmarks of the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a drastically reduced feed intake by an unknown mechanism. To further elucidate this wasting syndrome, we followed the effects of a single large dose (100 μg/kg) of TCDD on the serum levels of several energy balance-influencing hormones, clinical chemistry variables, and hepatic aryl hydrocarbon receptor (AHR) expression in two rat strains that differ widely in their TCDD sensitivities, for up to 10 days. TCDD affected most of the analytes in sensitive Long-Evans rats, while there were few alterations in the resistant Han/Wistar strain. However, analyses of feed-restricted unexposed Long-Evans rats indicated several of the perturbations to be secondary to energy deficiency. Notable increases in ghrelin and glucagon occurred in TCDD-treated Long-Evans rats alone, which links these hormones to the wasting syndrome. The newly found energy balance regulators, insulin-like growth factor 1 and fibroblast growth factor 21 (FGF-21), appeared to function in concert in body weight loss-induced metabolic state, and FGF-21 was putatively linked to increased lipolysis induced by TCDD. Finally, we demonstrate a reverse set of changes in the AHR protein and mRNA response to TCDD and feed restriction, suggesting that AHR might function also as a physiological regulator, possibly involved in the maintenance of energy balance.

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Section: Resultsmentioning

confidence: 99%

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

Lindén

Lensu

Pohjanvirta

2014

IJMS

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“…Additionally, AHR-mediated ubiquitin ligase activity was found when investigating the crosstalk between AHR and sex hormone receptors, with AHR promoting polyubiquitination and subsequent 26S proteosomal degradation of steroid receptors (Ohtake et al 2007) after the ligand-activated AHR assembles a CUL4B-based atypical E3 ubiquitin ligase complex to mediate nongenomic signaling pathways. The estrogen and androgen receptors were reported as substrates for this E3 ubiquitin ligase activity (Brunnberg et al 2012;Ohtake and Kato 2012), which is believed to be one method for AHR's ability to crosstalk with steroid receptor pathways. Recently, b-catenin, a transcription factor active in the WNT signaling pathway, was also found to be ubiquitinated by activated AHR (Kawajiri et al 2009).…”

Section: Ahr Ligands Exposure and Relevance To Human Healthmentioning

confidence: 99%

A20

2018

Encyclopedia of Signaling Molecules

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“…Such action, in turn, predisposes to mutations, affects the formation of harmful metabolites, and disrupts endocrine metabolism. 14 − 16 Moreover, the TCDD-activated AhR interferes with the estrogen receptor function, thereby causing reproductive and behavioral disorders. 16 − 19 The most-known and well-described adverse effects of dioxins on human and animal organisms are chloracne, infertility, increased concentration of globulins, delayed immune response, and disruption in thyroid hormone concentration.…”

Section: Introductionmentioning

confidence: 99%

Xanthohumol Effect on 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Treated Japanese Quails in Terms of Serum Lipids, Liver Enzymes, Estradiol, and Thyroid Hormones

et al. 2020

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Dioxins are compounds classified as persistent organic pollutants, from which 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) is the most toxic to living organisms. TCDD is considered a carcinogen and has proinflammatory influence on animals and humans, promoting free radicals’ formation, and binding with the aryl hydrocarbon receptor (AhR) leads to expression of cytochrome p-450 genes that in turn predisposes to mutations. Natural flavonoids, in this case xanthohumol (XN), have been reported to attenuate TCDD toxicity through inhibition of the transformation of the AhR. Moreover, XN shows antioxidant properties. The aim of the study was to compare the effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin and XN on lipid, liver enzyme, estradiol, and thyroid enzyme levels in the serum of Japanese quails. Adult, six-month-old, Japanese quails were divided into eight groups according to treatment procedures. Serum levels of total cholesterol (TCh), high-density lipoproteins (HDLs), triglycerides (TGs), estradiol, triiodothyronine, and thyroxine, and activities of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase were measured. In comparison with the control group, 2,3,7,8-tetrachlorodibenzo- p -dioxin significantly decreased concentrations of serum HDLs and thyroid hormones and significantly increased the serum TCh level. Levels of serum TGs, liver enzymes, and estradiol were not changed after 2,3,7,8-tetrachlorodibenzo- p -dioxin treatment. Based on our data, XN treatment may also increase the levels of thyroid hormones. Moreover, the tested dioxin disrupts the liver function, especially changing lipids’ metabolism. Therefore, more studies are needed for better understanding the mechanism of toxic influence of 2,3,7,8-tetrachlorodibenzo- p -dioxin on key metabolic pathways and organs in living organisms.

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Functional Interactions of AHR with other Receptors

Cited by 6 publications

References 138 publications

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

A20

Xanthohumol Effect on 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Treated Japanese Quails in Terms of Serum Lipids, Liver Enzymes, Estradiol, and Thyroid Hormones

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