Free radicals with a long lifetime were observed in the leaves of two rice cultivars (Oryza sativa L.), Sasanishiki (UVB resistant) and Norin-1 (UVB sensitive), by electron spin resonance spectroscopy. The leaves of both cultivars grown with visible light show very similar ESR spectra composed of radical 1 (R1) and radical 2 (R2), which may be attributable to P₇₀₀ cation radicals in the reaction center of photosystem I, and tyrosine cation radicals in the reaction center of photosystem II, respectively. The ESR spectrum composed of R1 and R2 radicals in the leaves of Sasanishiki grown under visible light with supplemental UVB was similar to that in the plant grown without supplemental UVB. On the other hand, the amount of R2 radicals in the leaves of Norin-1 grown under visible light with supplemental UVB was significantly smaller than that in the plant grown without supplemental UVB. It is suggested that the loss of R2 radicals in Norin-1 upon UVB irradiation is related to the instability of the plant.

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We studied X-ray-induced delayed cell death, delayed giant cell formation and delayed chromosome aberrations in normal human embryo cells to explore the relationship between initial radiation damage and delayed effect appeared at 14 to 55 population doubling numbers (PDNs) after X-irradiation. The delayed effect was induced in the progeny of X-ray survivors in a dose-dependent manner and recovered with increasing PDNs after X-irradiation. Delayed plating for 24 h post-irradiation reduced both acute and delayed lethal damage, suggesting that potentially lethal damage repair (PLDR) can be effective for relieving the delayed cell death. The chromosome analysis revealed that most of the dicentrics (more than 90%) observed in the progeny of X-ray survivors were not accompanied with fragments, in contrast with those observed in the first mitosis after X-irradiation. The present results indicate that the potentiality of genetic instability is determined during the repair process of initial radiation damage and suggest that the mechanism for formation of delayed chromosome aberrations by radiation might be different from that of direct radiation-induced chromosome aberrations.

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Although the acceleration of bone regeneration by radiation has been reported, the mechanisms of action of radiation on bone are unclear. The present results indicate that ionizing radiation-stimulated differentiation could result from the generation of reactive oxygen species during radiation exposure. The free radical release is considered as the most important mechanism of bone effect by radiation treatment. In addition, we report that radiation induced transient activation of c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) activation and the transcription factor, AP-1. The JNK and AP-1 activation is mediated with radiation-released free radicals in ROS 17/2.8 osteoblasts. These results indicate that ionizing radiation at a single dose of up to 5 Gray stimulates differentiation of ROS 17/2.8 osteoblasts via free radial release which may affect JNK/SAPK and AP-1 activities.

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Accumulated external radiation doses of residents near the Semipalatinsk nuclear test site of the former USSR are presented as a results of study by the thermoluminescence technique for bricks sampled at several settlements in 1995 and 1996. The external doses that we evaluated from exposed bricks were up to about 100 cGy for resident. The external doses at several points in the center of Semipalatinsk City ranged from a background level to 60 cGy, which was remarkably high compared with the previously reported values based on military data.

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