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Polycyclic aromatic hydrocarbons: Stealth carcinogens?

  1. Author:
    Khan, Q. A.
    Vousden, K.
    Dipple, A.
    1. Year of Conference: 1997
  2. Conference Name: Annual Meeting of the American Association for Cancer Research
    1. 38
    2. Pages: A4287
  4. Type of Work: Meeting Abstract
  1. Abstract:

    Polycyclic aromatic hydrocarbons (PAH) are generated through the inefficient combustion of organic matter and are present throughout the environment. They are potent carcinogens in experimental animals in which they are metabolized to reactive dihydrodiol epoxides that react with cellular macromolecules and are known mutagens. Many mammalian cells respond to DNA damage by arresting in G1 (to permit repair of DNA damage prior to DNA replication) through a mechanism mediated by the tumor suppressor gene product, p53. In this work, flow cytometry studies indicated that two dihydrodiol epoxides did not elicit this response in either RKO or MCF-7 cells even though these cells arrested in G1 in response to Actinomycin D. Western blots showed that p53 levels in MCF-7 cells increased in response to both Actinomycin D and anti benzo[g]chrysene 11,12-dihydrodiol 13,14-epoxide treatment but the p53 in the latter case seemed unable to enhance the transcription of the p21 required to block the movement of cells into the S-phase. The inability of this p53-mediated cellular protection mechanism to be activated by the DNA damage induced by the PAH dihydrodiol epoxides may be a major contributor to the carcinogenic potency of this class of carcinogens.

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