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- W1489779959 abstract "Two cytochrome P4501A-dependent mechanisms of aryl hydrocarbon receptor(AhR) agonist toxicity were examined in the marine teleost scup (Stenotomus chrysops),alteration of arachidonic acid (AA) metabolism and production of reactive oxygen species(ROS).In scup hepatic microsomes, cytochrome P450s including CYP1A and CYP2B-likeproteins catalyzed regioselective metabolism of AA to eicosatrienoic andhydroxyeicosatetraenoic acids. Benzo[a]pyrene (BP) treatment induced liver microsomalAA metabolism, but that effect varied with season. Endogenous AA epoxides wererecovered from scup liver, heart, and kidney, and their composition in the liver was alteredby treatment with BP or 2,3,7,8-tetrachlorodibenzo-p-dioxin.In scup and mammals, the formation of ROS was stimulated by binding of3,3',4,4-tetrachlorobiphenyl (TCB) to CYP1A, apparently CYP1Al. Attack of that ROSinactivated scup CYP1A. ROS release and inactivation of CYP1A were stimulated only bysubstrates of CYP1A that are slowly metabolized. In vivo, 3,3',4,4',5-pentachlorobiphenyl (PeCB) potently induced CYP1A mRNA, protein and catalytic activityat low doses (0.01-0.1 mg/kg), suppressed induction of CYP1A protein and catalyticactivity at a high dose (1 mg/kg) and transiently induced oxidative stress in scup liver. Thesuppression of CYP1A induction was organ-dependent, with hepatic CYP1A being mostsusceptible to inactivation. The results suggest that ROS could be involved in the in vivosuppression of scup liver CYP1A by planar halogenated aromatic hydrocarbons.The reactive oxygen sensitive transcription factor, nuclear factor-KB (NF-KB), wascharacterized in scup. An NF-KB consensus binding sequence bound specifically to 3proteins in scup liver, heart and kidney. One protein was recognized by an antibody tomammalian p50. Injection alone appeared to activate NF-KB. BP did not increase theactivation ofNF-KB, and PeCB activated NF-KB in only 1 of 2 experiments.Last, CYP1A induction in endothelial cells of the American eel (Anguilla rostrata), asite which may be particularly susceptible to alterations in AA metabolism and ROSproduction, was described. Eel liver CYP1A responded to BP, 13-naphthoflavone andTCB in a dose-dependent fashion, and induction was correlated with hepatic inducerconcentration. Endothelial CYP1A was inducible in a number of organs and wasmetabolically active. In the rete mirabile, penetration of endothelial CYP1A inductionincreased with increasing dose of AhR agonists, corresponding with an increase in inducerconcentration. A transition from endothelial to epithelial staining occurred in the gill, heartand kidney at high inducer doses." @default.
- W1489779959 created "2016-06-24" @default.
- W1489779959 creator A5015152982 @default.
- W1489779959 date "1998-01-01" @default.
- W1489779959 modified "2023-09-23" @default.
- W1489779959 title "Involvement of Cytochrome P450 1A in the toxicity of aryl hydrocarbon receptor agonists : alteration arachidonic acid metabolism and production of reactive oxygen species" @default.
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