Involvement of Cytochrome P450 1A in the Toxicity of Aryl Hydrocarbon Receptor Agonists: Alteration of Arachidonic Acid Metabolism and Production of Reactive Oxygen Species.

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-like proteins catalyzed regioselective metabolism of AA to eicosatrienoic and hydroxyeicosatetraenoic acids. BenzoApyrene (BP) treatment induced liver microsomal AA metabolism, but that effect varied with season. Endogenous AA epoxides were recovered from scup liver, heart, and kidney, and their composition in the liver was altered by treatment with BP or 2,3,7,8-tetrachlorodibenzo-p-dioxin. In scup and mammals, the formation of ROS was stimulated by binding of 3,3',4,4-tetrachlorobiophenyl (TCB) to CYP1A, apparently CYP1A1. Attack of that ROS inactivated scup CYP1A. ROS release and inactivation of CYP1A were stimulated only by substrates of CYP1A that are slowly metabolized. In vivo, 3,3',4,4',5-pentachlorobiphenyl (PeCB) potently induced CYP1A mRNA, protein and catalytic activity at low doses (0.01-0.1 mg/kg), suppressed induction of CYP1A protein and catalytic activity at a high dose (1 mg/kg) and transiently induced oxidative stress in scup liver. The suppression of CYP1A induction was organ-dependent, with hepatic CYP1A being most susceptible to inactivation. The results suggest that ROS could be involved in the in vivo suppression of scup liver CYP1A by planar halogenated aromatic hydrocarbons. The reactive oxygen sensitive transcription factor, nuclear factor-kB (NF-kB), was characterized in scup. An NF-KB consensus binding sequence bound specifically to 3 proteins in scup liver, heart and kidney. One protein was recognized by an antibody to mammalian p50. Injection alone appeared to activate NF-kB. BP did not increase the activation of NF-kB, and PeCB activated NF-kB in only 1 of 2 experiments.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Sep 01, 1998
Accession Number
ADA363733

Entities

People

  • Jennifer J. Schlezinger

Organizations

  • Woods Hole Oceanographic Institution

Tags

DTIC Thesaurus Topics

  • Birds
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Fish
  • Organic Chemistry
  • Wildlife

Fields of Study

  • Biology
  • Chemistry

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Toxicology/Environmental Toxicology