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Title: Cell-cycle radiation response: Role of intracellular factors

Technical Report ·
OSTI ID:7164944

The quantitative understanding of long-term effects of the components of space radiation on carcinogenesis and nervous-system functions depends on the nature of the molecular injury produced by particles of various atomic numbers and energies. Of particular interest is the functional dependence of individual lesions, their repair and misrepair, and the time-dependent interactions that can occur at low dose rates. Both inherited genetic susceptibility as well as normal programmed genetic functions occurring during cell division could contribute to the vulnerability of cellular targets to damage from ionizing radiations. The authors have studied variations of radiosensitivity and endogenous cellular factors during the course of progression through the human and hamster cell cycle. After exposure to low-LET radiations, the most radiosensitive cell stages are mitosis and the G1/S interface. The increased activity of a specific antioxidant enzyme such as superoxide dismutase in G1-phase, and the variations of endogenous thiols during cell division are thought to be intracellular factors of importance to the radiation-survival response. These factors may contribute to modifying the age-dependent yield of lesions or more likely, to the efficiency of the repair processes. Hazards posed by the interaction of damage from sequential doses of radiations of different qualities have been evaluated and are shown to lead to a cell-cycle-dependent enhancement of radiobiological effects. A summary comparison of various cell-cycle-dependent endpoints measured with low- or high-LET radiations is given and includes a discussion of the possible additional effects introduced by microgravity.

Research Organization:
Armed Forces Radiobiology Research Inst., Bethesda, MD (USA)
OSTI ID:
7164944
Report Number(s):
AD-A-214331/1/XAB; AFRRI-SR-89-27
Resource Relation:
Other Information: Pub. in Adv. Space Res., Vol. 9, No. 10, (10)177-(10)186(1989)
Country of Publication:
United States
Language:
English