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Significance of basic and clinical research in radiation medicine: challenges for the future

Heinrich-Heine-University Düsseldorf, Germany and Brookhaven National Laboratory, Upton, NY, USA

View larger version (42K): [in a new window]   Figure 1. Ionising radiation is a toxin to specific targets. Cells trigger tissue effects that vary with types of target response. Effects in cells and tissues depend on the degree of system perturbation. Low perturbations initiate adaptive responses; high perturbations bring damage or death. Note that radiation effects are partly comparable with effects of reactive oxygen species (ROS).

View larger version (29K): [in a new window]   Figure 2. Generation of reactive oxygen species by normal mammalian cells. (person. comm. S Orrenius, 2000).

View larger version (29K): [in a new window]   Figure 3. Risk per human stem cell per 1 mGy from 100 kV X-rays. D, absorbed dose; ROS, reactive oxygen species; DSB, double-strand breaks.

View larger version (25K): [in a new window]   Figure 4. DNA alterations per cell per day from low dose irradiation and from endogenous metabolic sources. ROS, reactive oxygen species; DSB, double-strand breaks.

View larger version (64K): [in a new window]   Figure 5. Effects of reactive oxygen species (ROS) in mammals on cell structure and function. DSB, double-strand breaks. (person. comm. S Orrenius, 2000).

View larger version (27K): [in a new window]   Figure 6. (a) Cell responses to oxidative stress. (b) Summary of responses. ROS, reactive oxygen species.

View larger version (24K): [in a new window]   Figure 7. Relationship of level of reactive oxygen species (ROS) and apoptosis in cells: caspase activation and inactivation for apoptosis. (person. comm. S Orrenius, 2000).

View larger version (33K): [in a new window]   Figure 8. Schematic presentation of dose–effect curves for adaptive protection, except for apoptosis, induced by low dose low-LET (linear energy transfer) radiation exposure.

View larger version (25K): [in a new window]   Figure 9. Schematic presentation of duration of adaptive protections. ROS, reactive oxygen species.

View larger version (26K): [in a new window]   Figure 10. Dual effect of low dose radiation on cellular DNA damage induction and adaptive protection, except for apoptosis.

View larger version (42K): [in a new window]   Figure 11. Relationship between dose rate and the average time interval between two consecutive events that bring a given dose to the affected nanogram of tissue, here called microdose , depending on radiation quality. ROS, reactive oxygen species. The figure also lists the dose-rate-dependent frequency of events within 100 ng, i.e. cells, per day. NH is the number of microdose events in exposed micromasses.

View larger version (44K): [in a new window]   Figure 12. Absorbed dose D expresses concentration not amount of energy E in mass M.

View larger version (39K): [in a new window]   Figure 13. Absorbed dose D is the sum of energy absorbed in exposed micromasses.

View larger version (46K): [in a new window]   Figure 14. Tissue response to radiation of a given quality derives from all cellular response probabilities per microdose event of size . In this simplified scheme: pspo is the probability of spontaneous cancer developing from an exposed micromass; pind is the probability of radiation-induced cancer, which is taken to be constant per microdose event in the low dose range; pprot is the probability of low dose specific protection against cancer, which changes with NH and tp; papo is the probability of radiation-induced apoptosis, which is taken to be constant per microdose event in the low dose range; tp is the time of duration of protection; NH is the number of microdose events in exposed micromasses; and NE is the number of exposed micromasses (see also Figure 13).

View larger version (38K): [in a new window]   Figure 15. Biological systems such as mammalian organisms maintain homeostatic equilibrium through signalling at all levels of biological organisation. These signals originate from various sites: those that control the entire organism, specific tissue functions, defined cell functions and intracellular functions. The signals always involve cell responses that govern various levels of biological organisation. The signalling serves to secure system integrity and survival in the face of perturbations constantly brought about by exposure to a multitude of endogenous and environmental toxic agents. Small and moderate degrees of perturbations tend to initiate adaptive responses, whereas severe perturbations may lead to system failure and death.