CYP1A in TCDD toxicity and in physiology - With particular reference to CYP dependent arachidonic acid metabolism and other endogenous substrates Review uri icon

Overview

MeSH Major

  • Arachidonic Acid
  • Cytochrome P-450 Enzyme System
  • Environmental Pollutants
  • Polychlorinated Dibenzodioxins

abstract

  • Toxicologic and physiologic roles of CYP1A enzyme induction, the major biochemical effect of aryl hydrocarbon receptor activation by TCDD and other receptor ligands, are unknown. Evidence is presented that CYP1A exerts biologic effects via metabolism of endogenous substrates (i.e., arachidonic acid, other eicosanoids, estrogens, bilirubin, and melatonin), production of reactive oxygen, and effects on K(+) and Ca(2+) channels. These interrelated pathways may connect CYP1A induction to TCDD toxicities, including cardiotoxicity, vascular dysfunction, and wasting. They may also underlie homeostatic roles for CYP1A, especially when transiently induced by common chemical exposures and environmental conditions (i.e., tryptophan photoproducts, dietary indoles, and changes in oxygen tension).

publication date

  • May 24, 2006

Research

keywords

  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1080/03602530600570107

PubMed ID

  • 16684662

Additional Document Info

start page

  • 291

end page

  • 335

volume

  • 38

number

  • 1-2