Literature DB >> 2834195

Ah receptor: relevance of mechanistic studies to human risk assessment.

J C Cook1, K W Gaido, W F Greenlee.   

Abstract

Studies of the toxic actions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in numerous animal models and in human and animal cells in culture have established that the most characteristic pathologic lesions produced by this compound result from events initiated by the interaction of TCDD with a specific intracellular receptor protein, the Ah receptor. Although most research on the interaction of TCDD with the Ah receptor has focused on establishing involvement of this receptor complex in specific toxic responses, recent application of modern cell and molecular biology techniques is yielding new insights into the mechanism(s) of signal transduction. Elucidation of these mechanisms is essential for understanding the molecular basis of the cell and species specificity which is a hallmark of TCDD toxicity. This knowledge should provide the framework for development of a more toxicologically relevant risk assessment model.

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Year:  1987        PMID: 2834195      PMCID: PMC1474477          DOI: 10.1289/ehp.877671

Source DB:  PubMed          Journal:  Environ Health Perspect        ISSN: 0091-6765            Impact factor:   9.031


  31 in total

1.  Isolation of an evolutionarily conserved epidermal growth factor receptor cDNA from human A431 carcinoma cells.

Authors:  F A Simmen; M L Gope; T Z Schulz; D A Wright; G Carpenter; B W O'Malley
Journal:  Biochem Biophys Res Commun       Date:  1984-10-15       Impact factor: 3.575

2.  Causal agents of yusho.

Authors:  N Kunita; T Kashimoto; H Miyata; S Fukushima; S Hori; H Obana
Journal:  Am J Ind Med       Date:  1984       Impact factor: 2.214

3.  Response of murine epidermis to 2,3,7,8-tetrachlorodibenzo-p-dioxin: interaction of the ah and hr loci.

Authors:  J C Knutson; A Poland
Journal:  Cell       Date:  1982-08       Impact factor: 41.582

4.  Immunosuppressive effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in strains of mice with different susceptibility to induction of aryl hydrocarbon hydroxylase.

Authors:  A Vecchi; M Sironi; M A Canegrati; M Recchia; S Garattini
Journal:  Toxicol Appl Pharmacol       Date:  1983-05       Impact factor: 4.219

5.  Increased epidermal transglutaminase activity following 2,3,7,8-tetrachlorodibenzo-p-dioxin: in vivo and in vitro studies with mouse skin.

Authors:  S M Puhvel; D C Ertl; C A Lynberg
Journal:  Toxicol Appl Pharmacol       Date:  1984-03-30       Impact factor: 4.219

6.  Reversible inhibition of in vitro epithelial cell proliferation by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Authors:  J F Gierthy; D Crane
Journal:  Toxicol Appl Pharmacol       Date:  1984-06-15       Impact factor: 4.219

7.  Control of cytochrome P1-450 gene expression by dioxin.

Authors:  P B Jones; D R Galeazzi; J M Fisher; J P Whitlock
Journal:  Science       Date:  1985-03-22       Impact factor: 47.728

8.  Sensitivity to suppression of cytotoxic T cell generation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is dependent on the Ah genotype of the murine host.

Authors:  P S Nagarkatti; G D Sweeney; J Gauldie; D A Clark
Journal:  Toxicol Appl Pharmacol       Date:  1984-01       Impact factor: 4.219

9.  2,3,7,8-Tetrachlorodibenzo-p-dioxin induces hyperplasia in confluent cultures of human keratinocytes.

Authors:  L M Milstone; J F LaVigne
Journal:  J Invest Dermatol       Date:  1984-05       Impact factor: 8.551

10.  Fetal thymus organ culture as an in vitro model for the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin and its congeners.

Authors:  L Dencker; E Hassoun; R d'Argy; G Alm
Journal:  Mol Pharmacol       Date:  1985-01       Impact factor: 4.436

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  1 in total

Review 1.  Environmental toxicology of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans.

Authors:  J P Vanden Heuvel; G Lucier
Journal:  Environ Health Perspect       Date:  1993-04       Impact factor: 9.031

  1 in total

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