Astaxanthin can alter CYP1A-dependent activities via two different mechanisms: induction of protein expression and inhibition of NADPH P450 reductase dependent electron transfer

Food Chem Toxicol. 2011 Jun;49(6):1285-91. doi: 10.1016/j.fct.2011.03.009. Epub 2011 Mar 23.

Abstract

Astaxanthin (Ax), a xanthophyll carotenoid, is reported to induce cytochrome P450 (CYP) 1A-dependent activity. CYP1A is one of the most important enzymes participating in phase I metabolism for chemicals, and it can activate various mutagens. To investigate the effect of Ax on the metabolic activation of a typical promutagen, benzo[a]pyrene by CYP1A, we orally administrated Ax-containing oil (100 mg Ax/kg body weight/day for 3 days) to male Wistar rats. In the treated rat liver, expression of CYP1A1 mRNA, protein, and its activity were significantly increased (5.5-, 8.5-, and 2.5-fold, respectively). In contrast, the activities of phase II enzymes (glutathione S-transferase and glucuronosyl-transferase) were not modulated by Ax-containing oil. As a consequence, the mutagenicity of benzo[a]pyrene was more enhanced in Ax-treated rats, compared with controls in the Ames assay. On the other hand, NADPH P450 reductase activity was decreased in liver microsomes from the treated group. This result suggests the possibility that Ax inhibits the electron supply necessary for CYP catalytic activities and decreases CYP1A activity indirectly. In conclusion, Ax-containing oil intake can alter CYP1A-dependent activities through two different mechanisms: (1) induction of CYP1A1 mRNA, protein expression, and activity; and (2) inhibition of the electron supply for the enzyme.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimutagenic Agents / pharmacology*
  • Benzo(a)pyrene / toxicity
  • Cytochrome P-450 CYP1A1 / antagonists & inhibitors*
  • Cytochrome P-450 CYP1A1 / biosynthesis
  • Cytochrome P-450 CYP1A1 / genetics
  • Electron Transport / genetics
  • Enzyme Inhibitors / pharmacology*
  • Fibrinolytic Agents / pharmacology*
  • Gene Expression Regulation, Enzymologic / drug effects
  • Glucuronosyltransferase / antagonists & inhibitors
  • Glucuronosyltransferase / genetics
  • Glucuronosyltransferase / metabolism
  • Glutathione Transferase / antagonists & inhibitors
  • Glutathione Transferase / genetics
  • Glutathione Transferase / metabolism
  • Liver / drug effects
  • Liver / enzymology
  • Male
  • Mutagens / toxicity
  • NADPH-Ferrihemoprotein Reductase / antagonists & inhibitors*
  • NADPH-Ferrihemoprotein Reductase / genetics
  • NADPH-Ferrihemoprotein Reductase / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Xanthophylls / pharmacology

Substances

  • Antimutagenic Agents
  • Enzyme Inhibitors
  • Fibrinolytic Agents
  • Mutagens
  • RNA, Messenger
  • Xanthophylls
  • Benzo(a)pyrene
  • astaxanthine
  • Cytochrome P-450 CYP1A1
  • NADPH-Ferrihemoprotein Reductase
  • Glucuronosyltransferase
  • Glutathione Transferase