Hepatic metabolism of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the rat and guinea pig☆
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Cited by (46)
Time-dependent transcriptomic and biochemical responses of 6-formylindolo[3,2-b]carbazole (FICZ) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are explained by AHR activation time
2016, Biochemical PharmacologyCitation Excerpt :2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant and carcinogen [19], is one of the most potent and studied ligands of the AHR. Unlike FICZ, TCDD and other dioxin-like compounds (DLCs) are metabolized very slowly [18,39,58]. Interestingly, FICZ has a higher AHR binding affinity than TCDD [44,45] and, in cells transiently transfected with avian AHRs, it induces AHR-mediated luciferase reporter gene activity with greater potency than TCDD (41- to 1534-fold more potent; [11]).
Behaviour of dioxin in pig adipocytes
2005, Food and Chemical ToxicologyBiodegradation of polychlorinated dibenzo-p-dioxins by recombinant yeast expressing rat CYP1A subfamily
2002, Archives of Biochemistry and BiophysicsCitation Excerpt :These results indicate that rat CYP1A2 can catalyze the hydroxylation with elimination of chloride substitution towards 2,3,7-TriCDD. In the last two decades, the metabolism of PCDDs has been studied using experimental animals and their hepatocytes [1–6]. Major metabolites were hydroxylated products, glucuronide conjugates, and sulfate conjugates [2,4].
Molecular cloning of cDNA for guinea pig CYP1A2 comparison with guinea pig CYP1A1
1997, Archives of Biochemistry and Biophysics
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Portions of this research were presented at the meetings of the American Society for Pharmacology and Experimental Therapeutics [The Pharmacologist (1984) 26, 232] and at the 4th International Symposium on Chlorinated Dioxins and Related Compounds, Ottawa, Canada, October 16–18, 1984.