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Related Experiment Videos

Increased somatic cell mutant frequency in atomic bomb survivors.

M Hakoda1, M Akiyama, S Kyoizumi

  • 1Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.

Mutation Research
|September 1, 1988
PubMed
Summary

Atomic bomb survivors showed higher frequencies of mutant T-cells lacking hypoxanthine guanine phosphoribosyltransferase (HPRT) activity compared to controls. This HPRT mutation in T-cells was detectable 40 years post-exposure, correlating with radiation dose.

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Area of Science:

  • Human genetics
  • Radiation biology
  • Immunology

Background:

  • Atomic bomb survivors provide a unique cohort for studying long-term radiation effects.
  • Hypoxanthine guanine phosphoribosyltransferase (HPRT) deficiency in T-cells is a marker for in vivo mutations.
  • Previous studies established methods for quantifying mutant T-cell frequencies.

Purpose of the Study:

  • To determine the frequency of mutant T-cells deficient in HPRT activity in atomic bomb survivors.
  • To assess the correlation between radiation dose and HPRT mutant T-cell frequency.
  • To evaluate the persistence of radiation-induced mutations in human T-cells over time.

Main Methods:

  • Direct clonal assay to determine mutant T-cell frequencies in peripheral blood.

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  • Comparison of mutant frequencies between exposed survivors (more than 1 rad) and controls (less than 1 rad).
  • Analysis using both tentative (T65D) and revised (DS86) radiation dose estimates.
  • Main Results:

    • Exposed survivors exhibited significantly higher mean mutant T-cell frequencies (5.2 x 10^-6) than controls (3.4 x 10^-6).
    • No significant correlation was found initially between mutant frequencies and T65D dose estimates.
    • Reanalysis with DS86 dose estimates revealed a significant, albeit shallow, positive correlation between T-cell mutant frequency and radiation dose.

    Conclusions:

    • In vivo HPRT mutations in human T-cells can be detected in atomic bomb survivors up to 40 years after exposure.
    • The DS86 dosimetry system provides a better correlation with T-cell mutation frequency than T65D.
    • This study validates the use of HPRT-deficient T-cells as a biomarker for long-term radiation exposure effects.