Abstract
Radiation cytogenetics has rich history and goes back over 70 years since its inception when McClintock (1931) integrated the radiation-induced mutations of Muller (1927) and Stadler (1928) into chromosome aberrations. Studies on the effects of radiation on chromosomes in the 1930s constituted the bases of later biophysical modeling such as target theory of Lea (1946), dual radiation action theory of Kellerer and Rossi (1972) and threshold energy model of Goodhead (1982). Coupled with the advancement in the molecular biology, cytogenetic technology, radiation sources and computer sciences, the classical theories of breakage-reunion hypothesis of Sax (1938), exchange hypothesis of Revell (1958) and track structure model of Neary (1965) have continued to be a major concern in the more modern understanding of the action of radiation on living cells. In particular, the introduction of human cell culture technology in the 1960s was epoch making in bridging laboratory science and science of human radiation exposures. The expansion of radiation cytogenetics has revealed several controversies as well, which have been a matter of current debate. However, these controversies must have a unified explanation. Indeed, we are now indubitably aware that the DNA double-strand breaks are the integral molecular species of the induction of chromosome aberrations by radiation. When the diverse cytogenetic observations are reviewed in orderly interpretation in the context of their reaction kinetics and double-strand break repair pathways specific to the DNA turnover cycle, the many of the controversies may be understood in a unified model.
