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Research Article Free access | 10.1172/JCI116089

Retinoid protection against x-ray-induced chromatid damage in human peripheral blood lymphocytes.

K K Sanford, R Parshad, F M Price, R E Tarone, and K H Kraemer

Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.

Find articles by Sanford, K. in: PubMed | Google Scholar

Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.

Find articles by Parshad, R. in: PubMed | Google Scholar

Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.

Find articles by Price, F. in: PubMed | Google Scholar

Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.

Find articles by Tarone, R. in: PubMed | Google Scholar

Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.

Find articles by Kraemer, K. in: PubMed | Google Scholar

Published November 1, 1992 - More info

Published in Volume 90, Issue 5 on November 1, 1992
J Clin Invest. 1992;90(5):2069–2074. https://doi.org/10.1172/JCI116089.
© 1992 The American Society for Clinical Investigation
Published November 1, 1992 - Version history
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Abstract

Oral administration of isotretinoin (13-cis retinoic acid) was shown previously (Kraemer, K. H., J. J. DiGiovanna, A. N. Moshell, R. E. Tarone, and G. L. Peck. 1988. N. Engl. J. Med. 318:1633-1637) to reduce the frequency of skin cancers in xeroderma pigmentosum (XP) patients. The mechanism of protection was unclear. In the present study, x-ray-induced chromatid damage in PHA-stimulated blood lymphocytes from five XP patients receiving isotretinoin was approximately half that in blood samples from the same patients before or subsequent to treatment. The x-ray-induced chromatid damage in blood lymphocytes from a normal control was reduced significantly by cocultivation with blood or plasma from an XP patient receiving isotretinoin or by addition of 10(-6) M isotretinoin to cultures 1 h before x-irradiation. A similar reduction in x-ray-induced chromatid damage was reported previously by adding to the culture medium, mannitol, a scavenger of the free hydroxyl radical, or catalase, which decomposes hydrogen peroxide; both of these products are generated during ionizing radiation. The present observations suggest that isotretinoin acts as a scavenger of such radiation products, thereby providing protection against x-ray-induced chromatid damage.

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