ABSTRACT
The quadratic coefficient of the dose response for double strand breaks arises from the conversion of a ‘first’ single strand break to a double strand break by a ‘secondary’ event caused by an independent ionisation track. At low-dose rate, the reduced biological effect that is relevant for radiological risk assessment, results from the cell’s ability to repair deoxyribonucleic acid (DNA) single strand breaks perfectly during an extended exposure. The explanation for this sparing effect is based on the perfect repair of ‘first’ DNA single strand breaks during exposure before they are converted to DNA double strand breaks. It is important to realise that this repair process is, indeed, perfect and there is no influence of the repaired single strand breaks on the cellular effects or on the shape of the dose–effect curves. The repair of both DNA single strand breaks and DNA double strand breaks can influence the number of double strand breaks which are induced and remain biologically effective.
