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1 December 2004 Relative Sensitivities of Repair-Deficient Mammalian Cells for Clonogenic Survival after α-Particle Irradiation
Mark A. Hill, M. Trent Herdman, David L. Stevens, Nigel J. Jones, John Thacker, Dudley T. Goodhead
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Abstract

Hill, M. A., Herdman, M. T., Stevens, D. L., Jones, N. J., Thacker, J. and Goodhead, D. T. Relative Sensitivities of Repair-Deficient Mammalian Cells for Clonogenic Survival after α-Particle Irradiation. Radiat. Res. 162, 667–676 (2004).

The clonogenic survival of cells of the radiation-sensitive hamster cell lines irs1, irs2, irs3 and xrs5, representing different DNA repair pathways, was compared to that of their parent lines after α-particle irradiation. Measurements of nuclear area were made to calculate the probability of surviving a single α-particle traversal, the average number of lethal lesions per track and per unit dose, along with the “intrinsic radiosensitivity” of these cells, allowing for the potential of multiple lethal lesions per traversal. For all cell lines studied, α particles were found to be more biologically effective per unit absorbed dose than X rays at inducing cell inactivation. The repair-deficient cells showed an enhanced sensitivity to α particles compared to their parent line, but the degree of enhancement was less than for X rays. The reduction in additional sensitivity for α-particle irradiation was shown not to be due predominantly to differences in cell geometry limiting the probability of a cell nucleus being traversed. The results suggest that both the nonhomologous end-joining pathway and to a lesser extent the homologous recombination repair pathway play a role in successful repair of α-particle-induced damage, although a large proportion of damage is not repaired by either pathway.

Mark A. Hill, M. Trent Herdman, David L. Stevens, Nigel J. Jones, John Thacker, and Dudley T. Goodhead "Relative Sensitivities of Repair-Deficient Mammalian Cells for Clonogenic Survival after α-Particle Irradiation," Radiation Research 162(6), 667-676, (1 December 2004). https://doi.org/10.1667/RR3265
Received: 11 December 2003; Accepted: 1 July 2004; Published: 1 December 2004
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