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Journal of Environmental Pathology, Toxicology and Oncology

 

ISSN for PRINT: 0731-8898

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$672.00

Issues per year:

4

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2004, Volume23

Issue 3

  84 pages  

DOI: 10.1615/JEnvPathToxOncol.v23.i3   

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  • Prevention and Repair of DNA Damage by Selected Phytochemicals as Measured by Single Cell Gel Electrophoresis
  • Sutapa Chakraborty
    Department of Environmental Carcinogenesis and Toxicology, Chittaranjan National Cancer Institute, Kolkata, India

    Madhumita Roy
    Department of Environmental Carcinogenesis and Toxicology, Chittaranjan National Cancer Institute, Kolkata, India

    Rathindra Kumar Bhattacharya
    Department of Environmental Carcinogenesis & Toxicology, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700026, India


    ABSTRACT

    We assessed the ability of some natural products−namely, curcumin, resveratrol, indole-3-carbinol, and ellagic acid−to modify the DNA damaging ability of the alkylating carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in cultured Chinese hamster lung fibroblast cells (CH V-79). MNNG produced DNA single strand breaks in a dose- and time-dependent manner, as observed by increase in the tail moments of the comet, when the cells were subjected to alkaline single cell gel electrophoresis. When the cells were treated in the presence of each of the natural compounds, the DNA damage caused by MNNG was considerably reduced. This effect was found to be dose related. Preincubation of cells with each of these compounds individually afforded significant protection to DNA against damage caused by subsequent treatment with MNNG, indicating a true chemopreventive role of these substances. The most remarkable aspect of the present study was that all four compounds helped in the recovery of DNA damage by accelerating DNA repair efficiency in the damaged cells. This was further substantiated by the observation on unscheduled DNA synthesis. Our results suggest that these agents are chemopreventive by virtue of their ability to protect DNA as well as to induce DNA repair.

    DOI: 10.1615/JEnvPathToxOncol.v23.i3.50

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