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Related Experiment Video

Updated: Jun 19, 2026

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

Dietary curcumin enhances benzo(a)pyrene-induced apoptosis resulting in a decrease in BPDE-DNA adducts in mice.

Rachana Garg1, Girish Maru

  • 1Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Tata Memorial Centre, Kharghar, Navi Mumbai-410 208, India.

Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer
|October 13, 2009
PubMed
Summary

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Curcumin enhances the removal of DNA adducts caused by benzo[a]pyrene (B(a)P) in mice. This occurs by increasing the apoptosis, or programmed cell death, of damaged cells, not by diluting the adducts through DNA synthesis.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Cancer Research

Background:

  • Benzo[a]pyrene (B(a)P) is a polycyclic aromatic hydrocarbon found in environmental pollutants.
  • B(a)P metabolites can form DNA adducts, which are linked to cancer initiation.
  • Curcumin, a compound from turmeric, has shown potential in reducing DNA adduct formation.

Purpose of the Study:

  • To investigate the effect of curcumin on the persistence and disappearance of BPDE-DNA adducts in mouse tissues.
  • To determine if curcumin influences cell turnover and apoptosis in relation to DNA adducts.
  • To elucidate the mechanism by which curcumin affects DNA adduct levels in vivo.

Main Methods:

  • Mice were administered B(a)P and then divided into control and curcumin-treated groups.

Related Experiment Videos

Last Updated: Jun 19, 2026

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

  • BPDE-DNA adduct levels were measured in liver and lung tissues at various time points.
  • DNA synthesis rates (using 3H-thymidine incorporation) and apoptosis markers (p53, Bax, Bcl2, Caspase-3) were evaluated.

    • Main Results:

    • A time-dependent decrease in BPDE-DNA adducts was observed in control mice.
    • Curcumin treatment led to a significantly greater reduction in DNA adducts compared to controls.
    • Increased apoptosis markers and decreased Bcl2 levels were observed in curcumin-treated mice, indicating enhanced apoptosis.
    • DNA synthesis rates were similar between control and curcumin groups, ruling out adduct dilution as the primary mechanism.

    Conclusions:

    • Curcumin post-treatment significantly enhances the disappearance of BPDE-DNA adducts in mouse tissues.
    • The enhanced adduct reduction is primarily mediated by curcumin-induced apoptosis of adducted cells.
    • Curcumin represents a potential therapeutic strategy for mitigating the genotoxic effects of B(a)P exposure.