Abstract

Germline mutation induction at mouse minisatellite loci by paternal low-dose (0.125–1 Gy) exposure to chronic (1.66×10 −4 Gy min −1) low-linear energy transfer (low-LET) γ-irradiation and high-LET fission neutrons (0.003 Gy min −1) was studied at pre-meiotic stages of spermatogenesis. Both types of radiation produced linear dose–response curves for mutation of the paternal allele. In contrast to previous results using higher doses, the pattern of induction of minisatellite mutation after chronic γ-irradiation was similar to acute (0.5 Gy min −1) exposure to X-rays, indicating that the elevated mutation rate was independent of the ability of the cell to repair damage induced immediately or over a period of up to100 h. Chronic exposure to fission neutrons was more effective than acute or chronic low-LET exposure (relative biological effectiveness, RBE=3.36). The data also provide strong support for the previous conclusion that increases in minisatellite mutation rate are not caused by radiation-induced DNA damage at minisatellite loci themselves, but rather from damage induced by ionising radiation elsewhere in the genome/cell.

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