Induction of the heme oxygenase gene in human skin fibroblasts by hydrogen peroxide and UVA (365 nm) radiation

evidence for the involvement of the hydroxyl radical

Stephen M Keyse, Rex M Tyrrell

    Research output: Contribution to journalArticle

    98 Citations (Scopus)

    Abstract

    The induction of heme oxygenase by both hydrogen peroxide and UVA (365 nm) radiation in normal human skin fibroblasts is prevented by prior treatment of cells with the specific iron chelators, o-phenanthroline or desferrioxamine. In addition, both iron chelators protected cells against the lethal effects of H2O2 treatment or UVA irradiation. We propose that the generation of the highly reactive hydroxyl radical by an iron catalyzed Fenton reaction is involved both in the induction of this stress response and, at least in part, in cell killing by the two treatments. These results are also consistent with the idea that the heme oxygenase gene is induced in response to oxidative stress and that its induction may constitute an inducible protective mechanism against oxidative damage induced by both hydrogen peroxide and UVA radiation.
    Original languageEnglish
    Pages (from-to)787-91
    Number of pages5
    JournalCarcinogenesis
    Volume11
    Issue number5
    DOIs
    Publication statusPublished - 1990

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    Heme Oxygenase (Decyclizing)
    Hydroxyl Radical
    Hydrogen Peroxide
    Iron
    Fibroblasts
    Radiation
    Chelating Agents
    Skin
    Genes
    Deferoxamine
    Oxidative Stress

    Cite this

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    title = "Induction of the heme oxygenase gene in human skin fibroblasts by hydrogen peroxide and UVA (365 nm) radiation: evidence for the involvement of the hydroxyl radical",
    abstract = "The induction of heme oxygenase by both hydrogen peroxide and UVA (365 nm) radiation in normal human skin fibroblasts is prevented by prior treatment of cells with the specific iron chelators, o-phenanthroline or desferrioxamine. In addition, both iron chelators protected cells against the lethal effects of H2O2 treatment or UVA irradiation. We propose that the generation of the highly reactive hydroxyl radical by an iron catalyzed Fenton reaction is involved both in the induction of this stress response and, at least in part, in cell killing by the two treatments. These results are also consistent with the idea that the heme oxygenase gene is induced in response to oxidative stress and that its induction may constitute an inducible protective mechanism against oxidative damage induced by both hydrogen peroxide and UVA radiation.",
    author = "Keyse, {Stephen M} and Tyrrell, {Rex M}",
    year = "1990",
    doi = "10.1093/carcin/11.5.787",
    language = "English",
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    pages = "787--91",
    journal = "Carcinogenesis",
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    TY - JOUR

    T1 - Induction of the heme oxygenase gene in human skin fibroblasts by hydrogen peroxide and UVA (365 nm) radiation

    T2 - evidence for the involvement of the hydroxyl radical

    AU - Keyse, Stephen M

    AU - Tyrrell, Rex M

    PY - 1990

    Y1 - 1990

    N2 - The induction of heme oxygenase by both hydrogen peroxide and UVA (365 nm) radiation in normal human skin fibroblasts is prevented by prior treatment of cells with the specific iron chelators, o-phenanthroline or desferrioxamine. In addition, both iron chelators protected cells against the lethal effects of H2O2 treatment or UVA irradiation. We propose that the generation of the highly reactive hydroxyl radical by an iron catalyzed Fenton reaction is involved both in the induction of this stress response and, at least in part, in cell killing by the two treatments. These results are also consistent with the idea that the heme oxygenase gene is induced in response to oxidative stress and that its induction may constitute an inducible protective mechanism against oxidative damage induced by both hydrogen peroxide and UVA radiation.

    AB - The induction of heme oxygenase by both hydrogen peroxide and UVA (365 nm) radiation in normal human skin fibroblasts is prevented by prior treatment of cells with the specific iron chelators, o-phenanthroline or desferrioxamine. In addition, both iron chelators protected cells against the lethal effects of H2O2 treatment or UVA irradiation. We propose that the generation of the highly reactive hydroxyl radical by an iron catalyzed Fenton reaction is involved both in the induction of this stress response and, at least in part, in cell killing by the two treatments. These results are also consistent with the idea that the heme oxygenase gene is induced in response to oxidative stress and that its induction may constitute an inducible protective mechanism against oxidative damage induced by both hydrogen peroxide and UVA radiation.

    U2 - 10.1093/carcin/11.5.787

    DO - 10.1093/carcin/11.5.787

    M3 - Article

    VL - 11

    SP - 787

    EP - 791

    JO - Carcinogenesis

    JF - Carcinogenesis

    SN - 0143-3334

    IS - 5

    ER -