An X-ray-induced protein in human T cell leukemia MOLT-4 cells is described. It was detected 4 hrs after irradiation by two dimensional gel electrophoresis and silver staining. The location is 41 kDa in the mass and 4.0 of pI. Its spots were collected from the gels and microsequenced. The protein was identified from its partial sequences as a set gene product, whose gene translocation previously was found in a case of acute undifferentiated leukemia. Polyclonal rabbit antibodies stained two spots, the 41 kDa (p 41) and the 42 kDa (p 42) proteins. Photoimage analyses of the silver-stained gels and Western blots indicated that the induction of p 41 was time dependent, starting 4 hrs after irradiation and reaching a plateau by 10 hrs, and was dose dependent between 1 and 10 Gy. p 41 appeared somewhat ahead of cell death, as determined by the dye exclusion test, but the role in that cell process has yet to be clarified.

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Effect of radon exposure on the activities of superoxide dismutase (SOD) in blood, kidney, liver and spleen of male Wistar rats were investigated. Radon exposure was carried out in a newly developed chamber with ²²⁶Ra as the radon source. SOD activity, measured by the spin trap method using an electron spin resonance spectrometer, increased greatly in liver and kidney after 4 hour exposure whereas it decreased significantly after 16 hour exposure. Despite approximately same total doses by the radon exposure, the stimulated SOD activity after 4 hour exposure was not observed after 16 hour exposure in kidney, liver and spleen except blood, suggesting that the stimulating effect could last for a short period.

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Molecular dynamics (MD) simulation of DNA dodecamer d(CGCGAATTC^*GCG)₂ with a primary radiation damage represented by 5-hydroxy-6-cytosinyl radical (C^*) in position 9 was performed with AMBER 4.0 force field with periodic boundary conditions for the solvent. The temperature, potential energy of the system, energetic contributions from groups and RMS deviation from original positions were examined throughout the course of the simulation up to 140 ps. The stabilized structure (after 100 ps) was distorted and bent near the damaged site, which is similar to that observed in the MD of DNA with thymine glycol (Miaskiewicz, K. et al (1994) Radiat. Protection Dosimetry, 52, 149-153). The results suggest that a small and local damage in DNA may cause a large and global conformational change in DNA. Water molecules form two layers at distance 2.5 Å and 5.5 Å around the DNA. The MD simulation is a new approach to study radiation damages in molecular level.

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Escherichia coli mutants which lack defence systems against such active oxygen forms as OxyR (ΔoxyR), superoxide dismutase (SOD) (sodA and sodB) and catalase (katE and katG) are sensitive to UV-A lethality under aerobic conditions, whereas OxyR- and SOD-mutants have resistance under anaerobic conditions and in the presence of sodium azide (NaN₃) during irradiation.
 UV-A induces lipid peroxidation in the ΔoxyR mutant, which is suppressed by NaN₃. These results suggest that UV-A generates ¹O₂ or the hydroxyl radical to produce lipid peroxides intracellularly in the ΔoxyR mutant and that O₂^- stress may be generated in the sodAB mutant after 8 hr of exposure to UV-A. The sensitivities of such DNA repair-deficient mutants as recA^ind- and uvrA to UV-A also were examined and compared. These mutants are sensitive to UV-A lethality under aerobic conditions but show only slight resistance under anaerobic conditions or in the presence of NaN₃ during irradiation. We conclude that NaN₃ protects these mutant cells from oxygen-dependent UV-A lethality.

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This paper describes the response of mouse small intestine, at several time points after treatment with neutron or X-irradiation, using doses expected to give similar effects in terms of crypt/microcolony survival. Using resin histology, the effects of radiation on the numbers of duodenal cell types and measurements of tissue areas were assessed. The results for individual parameters and for an estimate of overall damage are given in a data display, which summarises the morphological profile of the organ after both types of radiation.
 Damage and recovery were seen for many of the parameters studied but there was no standard response pattern applicable for all parameters. In particular, the response of individual crypt cell types could not be predicted from knowledge of the change in crypt numbers. With regard to the holistic response of the gut, neutron irradiation appeared to have caused more damage and produced more early effects than the X-irradiation. More specifically, neutron treatment led to more damage to the neuromuscular components of the wall, while X-irradiation produced early vascular changes.

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A previous study on mutagenesis by ²⁵²Cf radiation in mouse L5178Y cells showed that the frequency was higher when the dose was delivered chronically, which was in sharp contrast to the results by gamma-rays (Nakamura and Sawada, 1988). A subsequent study using synchronized cells revealed that the cells at G₂/M stage were uniquely sensitive to mutation induction by ²⁵²Cf radiation but not so by gamma-rays (Tauchi et al, 1993). We carried out the present study to test the possibility that radiation-induced G₂ block may be a major determinant of the inverse dose-rate effect following chronic ²⁵²Cf radiation.
 Growing cell population was first subjected to conditioning gamma or ²⁵²Cf radiation with different dose-rates, followed by cell cycle distribution analysis and ²⁵²Cf mutagenesis. We found that G₂/M fraction increased by 3- to 4-fold when the conditioning doses (2 Gy of gamma or 1 Gy of ²⁵²Cf radiation) were delivered chronically over 10 hours but only slightly so when the same doses were delivered for 1 hour or less. Subsequent ²⁵²Cf irradiation gave higher mutation frequencies in the cells pre-irradiated with gamma-rays over a protracted period of time than in those with higher dose-rate gamma-rays. These results suggest that radiation-induced G₂ block would be at least partly (but can not be totally) responsible for the inverse dose-rate effect.

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