Skip to main content
  • AACR Publications
    • Blood Cancer Discovery
    • Cancer Discovery
    • Cancer Epidemiology, Biomarkers & Prevention
    • Cancer Immunology Research
    • Cancer Prevention Research
    • Cancer Research
    • Clinical Cancer Research
    • Molecular Cancer Research
    • Molecular Cancer Therapeutics

AACR logo

  • Register
  • Log in
  • My Cart
Advertisement

Main menu

  • Home
  • About
    • The Journal
    • AACR Journals
    • Subscriptions
    • Permissions and Reprints
    • Reviewing
  • Articles
    • OnlineFirst
    • Current Issue
    • Past Issues
    • Meeting Abstracts
    • Collections
      • COVID-19 & Cancer Resource Center
      • Focus on Computer Resources
      • Highly Cited Collection
      • Editors' Picks
      • "Best of" Collection
  • For Authors
    • Information for Authors
    • Author Services
    • Early Career Award
    • Best of: Author Profiles
    • Submit
  • Alerts
    • Table of Contents
    • Editors' Picks
    • OnlineFirst
    • Citations
    • Author/Keyword
    • RSS Feeds
    • My Alert Summary & Preferences
  • News
    • Cancer Discovery News
  • COVID-19
  • Webinars
  • Search More

    Advanced Search

  • AACR Publications
    • Blood Cancer Discovery
    • Cancer Discovery
    • Cancer Epidemiology, Biomarkers & Prevention
    • Cancer Immunology Research
    • Cancer Prevention Research
    • Cancer Research
    • Clinical Cancer Research
    • Molecular Cancer Research
    • Molecular Cancer Therapeutics

User menu

  • Register
  • Log in
  • My Cart

Search

  • Advanced search
Cancer Research
Cancer Research
  • Home
  • About
    • The Journal
    • AACR Journals
    • Subscriptions
    • Permissions and Reprints
    • Reviewing
  • Articles
    • OnlineFirst
    • Current Issue
    • Past Issues
    • Meeting Abstracts
    • Collections
      • COVID-19 & Cancer Resource Center
      • Focus on Computer Resources
      • Highly Cited Collection
      • Editors' Picks
      • "Best of" Collection
  • For Authors
    • Information for Authors
    • Author Services
    • Early Career Award
    • Best of: Author Profiles
    • Submit
  • Alerts
    • Table of Contents
    • Editors' Picks
    • OnlineFirst
    • Citations
    • Author/Keyword
    • RSS Feeds
    • My Alert Summary & Preferences
  • News
    • Cancer Discovery News
  • COVID-19
  • Webinars
  • Search More

    Advanced Search

Regular Articles

Diosmin and Diosmetin Are Agonists of the Aryl Hydrocarbon Receptor That Differentially Affect Cytochrome P450 1A1 Activity

Henry P. Ciolino, Thomas T. Y. Wang and Grace Chao Yeh
Henry P. Ciolino
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Thomas T. Y. Wang
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Grace Chao Yeh
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
DOI:  Published July 1998
  • Article
  • Info & Metrics
  • PDF
Loading

Abstract

We investigated the effect of the chemopreventive compound diosmin and its aglycone form, diosmetin, on the carcinogen activation pathway mediated by the aryl hydrocarbon receptor (AhR) in MCF-7 human breast epithelial cancer cells. Treatment of the cells with diosmin caused a dose-dependent increase in the metabolism of the mammary carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), as assessed by increased formation of DMBA-DNA adducts and by DMBA-induced cytotoxicity. In contrast, treatment of the cells with diosmetin decreased both parameters. Diosmetin, but not diosmin, directly inhibited cytochrome P450 1A1 (CYP1A1) activity in a noncompetitive manner in microsomes isolated from DMBA-treated cells, as assayed by ethyoxyresorufin-O-deethylase activity. Treatment of the cells with diosmin or diosmetin, on the other hand, caused a dose- and time-dependent increase in CYP1A1 activity in intact cells that was comparable to that induced by DMBA or by the aryl hydrocarbon benzo(a)pyrene. Both diosmin and diosmetin caused an increase in the transcription of the CYP1A1 gene, as measured by increased levels of CYP1A1 mRNA. Both compounds caused the activation of the DNA-binding capacity of the AhR for the xenobiotic-responsive element of CYP1A1. These results indicate that diosmin and diosmetin are natural dietary agonists of the AhR, causing a potent increase in CYP1A1 transcription and CYP1A1 activity; however, only diosmetin is capable of inhibiting CYP1A1 enzyme activity, thus inhibiting carcinogen activation.

Footnotes

  • ↵1 To whom requests for reprints should be addressed, at Laboratory of Nutritional and Molecular Regulation, National Cancer Institute-Frederick Cancer Research and Development Center, Building 560/Room 12-05, P. O. Box B, Frederick, MD 21702-1201. Phone: (301) 846-5160; Fax: (301) 846-6093; E-mail: hciolino@mail.ncifcrf.gov.

  • Received January 13, 1998.
  • Accepted April 30, 1998.
  • ©1998 American Association for Cancer Research.
PreviousNext
Back to top
July 1998
Volume 58, Issue 13
  • Table of Contents
  • Table of Contents (PDF)
  • Back Matter (PDF)
  • Editorial Board (PDF)
  • Front Matter (PDF)

Sign up for alerts

Open full page PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for sharing this Cancer Research article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Diosmin and Diosmetin Are Agonists of the Aryl Hydrocarbon Receptor That Differentially Affect Cytochrome P450 1A1 Activity
(Your Name) has forwarded a page to you from Cancer Research
(Your Name) thought you would be interested in this article in Cancer Research.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Diosmin and Diosmetin Are Agonists of the Aryl Hydrocarbon Receptor That Differentially Affect Cytochrome P450 1A1 Activity
Henry P. Ciolino, Thomas T. Y. Wang and Grace Chao Yeh
Cancer Res July 1 1998 (58) (13) 2754-2760;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Diosmin and Diosmetin Are Agonists of the Aryl Hydrocarbon Receptor That Differentially Affect Cytochrome P450 1A1 Activity
Henry P. Ciolino, Thomas T. Y. Wang and Grace Chao Yeh
Cancer Res July 1 1998 (58) (13) 2754-2760;
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
  • Info & Metrics
  • PDF
Advertisement

Related Articles

Cited By...

More in this TOC Section

Regular Articles

  • Progression of Hepatic Neoplasms Is Severely Retarded in Mice Lacking the Bisecting N-Acetylglucosamine on N-Glycans: Evidence for a Glycoprotein Factor that Facilitates Hepatic Tumor Progression
  • Explaining Differences in Sensitivity to Killing by Ionizing Radiation between Human Lymphoid Cell Lines
  • p53 Genes Mutated in the DNA Binding Site or at a Specific COOH-terminal Site Exert Divergent Effects on Thyroid Cell Growth and Differentiation
Show more Regular Articles

Carcinogenesis

  • Abstract LB-091: Characterization of molecular changes occurring during long-term treatment of human bronchial epithelial cells with cigarette smoke total particulate matter
  • Abstract LB-088: Ptch1 heterozygosity predisposes mice to developing IR-induced BCCs
  • Abstract LB-092: Programmed death-ligand 1 is overexpressed in bronchial preneoplastic lesions: can it be a risk indicator
Show more Carcinogenesis

Articles

  • Abstract LB-091: Characterization of molecular changes occurring during long-term treatment of human bronchial epithelial cells with cigarette smoke total particulate matter
  • Abstract LB-088: Ptch1 heterozygosity predisposes mice to developing IR-induced BCCs
  • Abstract LB-092: Programmed death-ligand 1 is overexpressed in bronchial preneoplastic lesions: can it be a risk indicator
Show more Articles
  • Home
  • Alerts
  • Feedback
  • Privacy Policy
Facebook  Twitter  LinkedIn  YouTube  RSS

Articles

  • Online First
  • Current Issue
  • Past Issues
  • Meeting Abstracts

Info for

  • Authors
  • Subscribers
  • Advertisers
  • Librarians

About Cancer Research

  • About the Journal
  • Editorial Board
  • Permissions
  • Submit a Manuscript
AACR logo

Copyright © 2021 by the American Association for Cancer Research.

Cancer Research Online ISSN: 1538-7445
Cancer Research Print ISSN: 0008-5472
Journal of Cancer Research ISSN: 0099-7013
American Journal of Cancer ISSN: 0099-7374

Advertisement