Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin on the Expression of Cytochrome P450 1A1, the Aryl Hydrocarbon Receptor, and the Aryl Hydrocarbon Receptor Nuclear Translocator in Rat Brain and Pituitary

Huang, Ping; Rannug, Agneta; Ahlbom, Eva; Håkansson, Helen; Ceccatelli, Sandra

doi:10.1006/taap.2000.9064

Cited by 109 publications

(77 citation statements)

References 49 publications

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“…In support of this, AhR ligand increases the levels of gonadotropine II and adrenocorticotropic hormone produced in pituitary. [24][25][26] From reports above mentioned, one possibility with respect to the reducing mechanism of GGA is raised that GGA exerts its protective effects by affecting a target(s) located downstream of the AhR pathways.…”

Section: Discussionmentioning

confidence: 99%

Reduction of the Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Mice Using an Antiulcer Drug, Geranylgeranylacetone

Ishida

Oshimo

Nishimura

et al. 2004

Biological & Pharmaceutical Bulletin

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The protective effect of geranylgeranylacetone (GGA), an antiulcer drug, against the acute toxicity and teratogenicity produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was examined in C57BL/6J mice. When mice were co-treated, GGA reduced the loss of body weight gain and lethality produced by TCDD but hepatomegaly and thymic atrophy were not improved. Additionally, no protective effect of GGA was observed in the formation of cleft palate and hydronephrosis in mouse fetuses caused by maternal exposure to TCDD. To clarify the reducing mechanism by GGA, the Hsp70.1 mRNA levels in liver and intestine were analyzed. However, it was difficult to explain the effect of GGA from the induction of Hsp70.1. GGA had also no effect on the induction of hepatic ethoxyresorufin O-deethylase activity by TCDD. These data suggest that GGA exhibits a protective effect against some forms of dioxin toxicity by a mechanism without involving inhibition of arylhydrocarbon receptor activation.

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Section: Discussionmentioning

confidence: 99%

Reduction of the Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Mice Using an Antiulcer Drug, Geranylgeranylacetone

Ishida

Oshimo

Nishimura

et al. 2004

Biological & Pharmaceutical Bulletin

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“…The autographical study revealed that highest concentrations of 14 C-TCDD were found in the hypothalamus and the pituitary after the exposure 63) . The expression of CYP1A1 mRNA and proteins were observed 1 day after the exposure to TCDD (10 µg/kg in SD rats) in all regions of the brain 61) . These studies indicate that dioxins can be transferred to the brain and affect immediately after exposure, via AhR system.…”

Section: Ahreceptor Systemmentioning

confidence: 99%

“…Kainu et al (1995) has shown that AhR is expressed in neurons and glial cells 60) . A recent study revealed the expression of CYP1A1, AhR, and ARNT in the olfactory bulb, hypothalamus, hippocampus, neocortex, substantia nigra, cerebellum, and pituitary, by a semiquantitative assay by RT-PCR and western blotting 61) . Petersen et al (2000) reported that the in situ hybridization signals for AhR and ARNT were observed in the arcuate nucleus (Arc), ventromedial hypothalamus (VMH), periventricular nucleus (PVN), suprachiasmatic nucleus (SCN), dorsal raphe nucleus, and median raphe nucleus in SD rats, and that the levels of ARNT2 mRNA expression were greater than that of ARNT mRNA 62) .…”

Section: Ahreceptor Systemmentioning

confidence: 99%

Developmental Neurotoxicity of Dioxin and Its Related Compounds.

Kakeyama

Tohyama

2003

INDUSTRIAL HEALTH

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This manuscript reviewed the neurotoxicity of dioxins and related compounds with an emphasis on maternal exposure. The brain during developmental period is thought to be highly sensitive to dioxin and its related compounds that affect a broad range of brain functions from the advanced brain function to the reproduction-controlling function, even at low doses. It is suggested that dioxins exhibit endocrine-disrupting action on the gonadal and thyroid hormone axes, as well as the 'neural-disrupting action' on neural transmission and neural network formation. From behavioral toxicological studies as well as studies on the underlying mechanisms of dioxins' toxicity, dioxins affect some specific functions in particular regions or cells of the brain at critical windows during the developmental period.

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“…Previous studies demonstrated that PCDD/Fs and PCBs cause reproductive toxicity, immunotoxicity, or neurotoxicity via aryl hydrocarbon receptor-signaling cascades in organism ranging from invertebrates to mammals (Kerkvliet 1995;Grassman et al 1998;Huang et al 2000;Petroff et al 2001;Kakeyama & Tohyama 2003;Fox 2005;Mandal 2005). The majority of studies regarding the toxicological risk of dioxin-like compounds involve the analysis of organic pollutants and in vitro toxicity assays using physiological markers, such as the cytochrome P450 family in seabream (Ortiz-Delgado et al 2005), zebrafish embryos (Andreasen et al 2002), and mouse heap-1 cells (Rivera et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Characterization of proteins in the gonad of Limanda yokohamae from Masan Bay, Korea

Soo-Woon

Moon

et al. 2010

Biologia

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Abstract:The putative biological effects of the toxic organic pollutants polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and the dioxin-like polychlorinated biphenyls (DLPCBs) in the sediments of Masan Bay, Korea, on the gonad of Limanda yokohamae were investigated using proteomic and bioinformatic analyses. The results demonstrated that 11 protein spots from the bay site, Duckdong, were statistically different from the reference site Gaduck Island. We identified 20 proteins from the 11 altered protein spots and these were found to be involved in multi-cellular functions as previously demonstrated in a variety of species. The concentrations of toxic equivalents of PCDD/Fs and DLPCBs in the sediments of Masan Bay were approximately twenty six-fold higher than those from Gaduck Island. These findings indicate that the organic contaminants in the sediments of Masan Bay may have contributed to the change in the phenotypes of fish gonads.

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Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin on the Expression of Cytochrome P450 1A1, the Aryl Hydrocarbon Receptor, and the Aryl Hydrocarbon Receptor Nuclear Translocator in Rat Brain and Pituitary

Cited by 109 publications

References 49 publications

Reduction of the Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Mice Using an Antiulcer Drug, Geranylgeranylacetone

Reduction of the Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Mice Using an Antiulcer Drug, Geranylgeranylacetone

Developmental Neurotoxicity of Dioxin and Its Related Compounds.

Characterization of proteins in the gonad of Limanda yokohamae from Masan Bay, Korea

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