The effect of dimethyl sulphoxide on the induction and repair of double-strand breaks in human cells after irradiation with gamma-rays and accelerated ions: rapid or slow repair may depend on accessibility of breaks in chromatin of different compactness

Abstract

Purpose : The repair of double-strand breaks (dsb) in mammalian cells is characterized by a rapid phase with a half-life of less than half an hour and a slower phase that lasts for many hours. The proportion of slow repair increase with LET and it has been suggested that the slow repair component consists of more complex damage and is more deleterious to the cells. To see if removal of OH radicals could remove part of the damage in complex dsb and make them easier to repair, human cells were irradiated in the presence of dimethyl sulphoxide (DMSO). Methods : Induction and repair of dsb were studied by neutral elution in human VH10 cells exposed to gamma-rays, helium ions (mean LET 40 keV/mum) and 80 and 125 keV/mum monoenergetic nitrogen ions in the presence and absence of 2M DMSO. Results : Incubation of cells exposed to gamma-rays, 40 keV/mum helium and 80 keV/mum N ions demonstrated that scavenging of OH radicals by DMSO removed most of the rapid repair component. The response to DMSO was less marked after 125 keV/mum nitrogen ions, where about half of the rapid repair was resistant to DMSO. Conclusions : It is unlikely that the complexity of dsb is responsible for the slow repair because the removal of OH radicals did not make the breaks easier to repair. Instead, it is suggested that rapid and slow repair can be explained on the basis of how different parts of the chromatin are accessible to repair enzymes.