Recovery of a low mutant frequency after ionizing radiation-induced mutagenesis during spermatogenesis

Guogang Xu, Gabriel W. Intano, John R. McCarrey, Ronald B. Walter, C. Alex McMahan, Christi A. Walter

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Humans are exposed to ionizing radiation (IR) under various circumstances, e.g. cosmic radiation, diagnostic X-rays and radiotherapy for cancer. It has been shown that IR can impair spermatogenesis and can cause mutations in germ cells. However, the mutagenic responses of germ cells exposed to IR at different stages of testicular maturation have not been examined by directly assessing the mutant frequency in defined spermatogenic cell types. This study was performed to address whether preadult exposure to IR can increase mutations in adult germ cells that could in turn have a major impact on adult reproductive function and the health of ensuing offspring. Male Lac I transgenic mice were irradiated with a single dose of 2.5 Gy of γ-ray at different ages before adulthood, reflecting different stages of testicular maturation, and then mutant frequency (MF) was determined directly in spermatogenic cell types emanating from the irradiated precursor cells. The results showed that (1) preadult exposure to IR did not significantly increase MF in adult epididymal spermatozoa; (2) spermatogenic stages immediately following the irradiated stage(s) displayed an elevated mutant frequency; but (3) the mutant frequency was restored to unirradiated levels in later stages of spermatogenesis. These findings provide evidence that there is a mechanism(s) to prevent spermatogenic cells with elevated mutant frequencies from progressing through spermatogenesis.

Original languageEnglish (US)
Pages (from-to)150-157
Number of pages8
JournalMutation Research - Genetic Toxicology and Environmental Mutagenesis
Issue number2
StatePublished - Jul 31 2008


  • Ionizing radiation
  • Lac I mouse
  • Mutagenesis
  • Spermatogenic cells

ASJC Scopus subject areas

  • Genetics
  • Health, Toxicology and Mutagenesis


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