Low dose radiobiology: Mechanistic considerations

The question of whether very small doses of ionizing radiation really exert stochastic effects (i,e, induce harmful genetic effects, including cancer in a probablistic manner) has not been unequivocally settled. The much reli ed upon linear, no-threshold (LNT) hypothesis does not have convincing expe rimental evidence. As there are practical difficulties in generating data o n genetic effects at very low doses and low dose rates, the conceptual deve lopment of the LNT hypothesis has depended upon background extrapolations f rom observations at high doses to low dose-regions, The dose, dose rate as well as the quality of radiation exposures in the case of atomic-bomb survi vors and their descendants are fraught with uncertainties. With data accumu lating on radiation-induced gene expression, the basic concepts of how cell death is caused are undergoing significant changes. Many reported phenomen a such as 'radiation hormesis' and 'radioadaptive response' could no more b e outright rejected and these challenge the LNT hypothesis. The fact remain s that the LNT is an over simplistic 'biophysical model' to explain radiati on action on the DNA of living cells and organisms. It truly masks the whol e lot of physical, physicochemical, biochemical and metabolic events involv ing not just the DNA but also the myriads of small and large molecules, whi ch characterize the various organelles. Most fundamentally, the LNT ignores repair processes, immune reactions and the role of apoptosis. The purpose of this review is purely to address this issue from a scientific point of v iew and not to deal with implications for radiological protection standards .