Intestinal mucosal epithelial cells and lymphocytes were both severely injuried by radiation, which leaded to endogenous infection and intestinal dysfunction. The ralated mechanisms were approved that proliferating activity and cytotoxicity of intraepithelial lymphocytes decreased, meanwhile TNF-α and TGF-β genes expression increased, the quantity of plasma cells secreted IgA and IL-4 gene expression were depressed. On the other hand, necrosis or apoptosis of intestinal crypt cells, structure abnormality and deletion of villi leaded to intestinal dysfunction. Analyzed the gene profiles and protein expression of irradiated intestinal epithelium and observed that R1S1, a new gene, and R1S2 genes specially expressed after 3h, but R2S2 and R2S5 genes expressed after 96h. PrxI and ERP29 proteins induced by radiation high expressed and identified PrxI had a radioprotective function. 20kD protein isolated from burned serum, glucagons-like peptide-2, rhIL-4 and human defensin5 were effective to promote the recovery of intestinal mucosal immune and epithelia so decreasing the incidence of endogenous infection and restoring intestine function. [J Radiat Res 44:370 (2003)]

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A high-dose-rate (HDR) Co-60 brachytherapy was used in Maharaj-Nakorn-ChiangMai Hospital from 1986 to 2001. The five year survival rate of 1992 patients with carcinoma of the cervix treated with combined external beam radiation therapy (EBRT) and Co-60 HDR brachytherapy was reported in the year 2000. Ir-192 source was introduced in 2001 and the same treatment regimen was applied. We evaluated the incidence of late complication of 100 patients underwent the two HDR systems. The linear-quadratic (LQ) formula was used to calculate the biologically equivalent dose (BED) and reconverted to dose equivalent of fractionated irradiation at 2 Gy/fraction for simplicity. The a/b ratio of 10 Gy and 3 Gy were taken for tumor and late effect respectively and the late complication was scored according to RTOG late radiation morbidity scoring scheme. We found that for Co-60 HDR, the average BED10 and BED3 was 100.7 Gy and 94.5 Gy respectively corresponding to dose equivalent of 84.1 Gy and 56.7 Gy comparing to BED10 of 100.8 Gy and BED3 of 125.4 Gy for Ir-192 corresponding to dose equivalent of 84.1 Gy and 75.24 Gy, respectively. The complication was relatively higher in Ir-192 group but still comparable with other series. [J Radiat Res 44:370 (2003)]

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We established the correlation between the radiosensitivity and the Hprt gene mutant frequency (MF) of three nasopharyngeal carcinoma (NPC) cell lines. Cells in exponential phase (CG1 cells were from Taiwan, CNE1 cells were from China and HK1 cells were from Hong Kong) were irradiatied with 1, 2, 4 and 6 Gy. Irradiated cells were cultured for 9 days in non-selective medium to allow full phenotypic expression of induced mutants for mutagenesis assay. Cells were then replated into new medium containing 6-thioguanine (6-TG) to select for Hprt mutants. D10's (i.e. radiation dose for 10% surviving fraction) were 5.5 Gy, 6.8Gy and 7.0 Gy for CNE1, HK1 and CG1 cells, respectively. Induced MF was increased as radiation doses increased. The curves for MFs of three cell lines were 1.35D2+1.11D, 1.01D2+4.44D-1.1076, and 0.95D2+4.65D, respectively. CNE1 cells were the most radiosensitive among the three human NPC cell lines, however, hypomutability was also found with CNE1 cells. The dose response for the induction of deletion mutations best fit a quadratic dose response (r2=0.99, p=0.001). Exons deletions were found mostly at both ends of Hprt gene. Terminal deletions also were increased with radiation dose in quadratic mode (r2=0.99, p=0.0001). The dose response for intragenic deletions best fits linear dose response (r2=0.94, p=0.001). (This study was supported by a grant NSC 89-2314-B-010-053-M08 from National Scientific Council, Taiwan) [J Radiat Res 44:370 (2003)]

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The failure of therapeutic responsiveness to radiation of malignant brain tumors, glioblastomas, remains a significant clinical problem. Tumor suppressor p53, a guardian gene with multiple functions, has been found to contain mutations in more than 50% of high-grade gliomas. Two glioblastoma cell lines, U87 and U138, the latter possessing mutated p53, were used for investigation of the differences in cell survival, cell-cycle checkpoints, apoptotic debris after gamma irradiations. While subtle difference was shown between U87 and U138 in survival curve shape, their major difference was in the cell-cycle checkpoints. After 10 Gy irradiation, U87 exhibited progression perturbation in G1, S and G2, in contrast to those by U138 where a prolonged and stronger G2 arrest but little or no G1 and S checkpoints were indicated. Further, FCM showed more apoptotic debris after the release of the G2 arrest in U138 than in U87. To help elucidate the mechanisms of these cellular effects, we have conducted time-course experiments to measure global gene expression using high-density cDNA and oligonucleotide microarray, with qPCR validations. We will present the outcome of gene expression results with a focus on genes related to cell-cycle control and apoptosis. Based on these results and current knowledge on the molecular pathways of cell-cycle regulation, we propose a model on p53-independent G2 arrest pathways. Our preliminary analysis indicates that in the absence of TP53 function, its family members p63 and TP73 may serve its role to regulate down stream genes such as p21 and GADD45A leading to inactivation of the CyclinB/Cdc2 complex. The alternative pathways are apparently more effective in causing G2 blockade than the p53-dependent pathways and the model is subjected to further test at the protein level. This work is partially supported by Grants NSC91-3112-P-010-003-Y, NSC91-2314-B-010-042, and NHRI-EX92-9115SN. [J Radiat Res 44:371 (2003)]

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We traced the course of radiation induced genomic instability in mouse hemopoietic cells from fetus to adult. Fourteen-day pregnant mice were exposed to 0.5-1Gy 60Co gamma radiation. Chromosomal aberrations were scored in fetal liver cells and postnatal bone marrow up to 18 months of age. Fetal hemopoietic cells and their progeny (CFU-S) showed significantly high number of aberrant metaphases. Such increases were not found in the postnatal bone marrow up to 6 months of age. However, the incidence of metaphases with structural chromosomal aberrations and aneuploidy (hypo- and hyperploidy) increased progressively from 9 to 18 months of age. An interesting finding, not reported earlier, is the progressive increase in chromosome loss with abnormal increase in leukocyte counts. This study demonstrates that a single dose of <1Gy of γ-rays can induce significant genomic instability in the fetal hemopoietic cells, which is transmitted to the postnatal bone marrow and expressed as severe chromosome aneuploidy at advanced ages. This may have a bearing on cancer induction in adult by fetal irradiation. (Supported by the Council of Scientific and Industrial Research, Government of India). [J Radiat Res 44:371 (2003)]

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From a starving nation in 1947 when we got our independence, India has become self-sufficient in food. In Atomic Energy, India has achieved capabilities spanning the entire nuclear cycle i.e. from exploration, to production of fuel elements for reactors, to construction of power reactors, reprocessing of spent fuels and waste management. In Indian Space Research programme, with the launch of our first satellite "Aryabhata" to the launch of several series of INSAT satellites, has been a great achievement. In electronics, all the equipment presently required for air defence, consisting of radars of various types, troposcatter, cable and microwave communication links, data handling system are all of Indian manufacture. In oil and natural gas sector, there has been remarkable technological and manufacturing achievements across the entire spectrum. In health, the crude mortality rate has declined from 32 per 1000 population to less than 8 today; the infant mortality rate of 40 per 1000 live births has decreased from over 135. Life expectancy has risen from 32 years in 1947 to over 62 years now Achievements and short-comings of the Indian Science and technology will be discussed. [J Radiat Res 44:371 (2003)]

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The rat is an important murine model for radiation research. Through much work the rat genomic toolbox is almost full a key missing tool was the ability to produce knockout rats. In order to approach this problem we developed a unique technology that combined the use of germline mutagenesis with a yeast truncation gap repair assay to select gene-specific knockout rats. We first developed the protocols to efficiently mutagenize the rat genome with ENU. In order to establish knockout rats for specifically chosen genes, we bred ENU mutagenized males to untreated females to produce F1 pups. These pre-weanling pups were screened for functional mutations .This was accomplished using a highly efficient and economical yeast gap-repair truncation assay. PCR product of the targeted gene together with our reporter vector is co-transformed into yeast that do not express ADE2. The yeast through homologous recombination clone the PCR product into the ADE2 reporter plasmid. In scoring the yeast plates a negative has mostly white large colonies and a positive for a knockout allele have half red colonies rat and half white colonies. We have used this technology to knockout two breast cancer suppressor genes, Brca1 and Brca2. Both of these genes are important in the repair of radiation - DNA damage. [J Radiat Res 44:371-372 (2003)]

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Repair of ionizing radiation (IR) induced DNA DSBs shows two defined components, and is dominated by a fast component that requires the activities of DNA-PK, and DNA ligase IV/XRCC4 (D-NHEJ). Cells with defects in either DNA-PK, or DNA ligase IV complex rejoin the majorityof IR-induced DSBs utilizing an alternative pathway operating with slower kinetics that could reflect HDR. Yet, the hyper-recombinogenic DT40 chicken cell line and a set of mutants defective in homologous recombination (HR) rejoin DSB with kinetics similar to the wild type even when D-NHEJ is severely compromised. Thus, increase in the HR capacity of cells, or defects in the proteins involved, fail to alter the rejoining kinetics in a way compatible with an involvement of HDR in the slow component of rejoining. We propose therefore the operation of an alternative pathway operating as a backup and termed B-NHEJ. B-NHEJ operates in vitro independently of Ku or DNA-PKcs and requires a distinct ligase. Immunofluorescence studies however indicate prolonged Rad51 foci formation, compatible with a functional HDR. A model will be presented that recapitulates genetic and biochemical results, and addresses the processing ofIR-induced DNA DSBs by D-NHEJ, B-NHEJ and possibly HDR in the context of chromatin. [J Radiat Res 44:372 (2003)]

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RNA interference was discovered only five years ago and is now recognized as an important system for the control of gene expression. More recent studies of the nature of RNAi have opened many possibilities for its control, and its exploitation promises to be a valuable experimental tool as it allows investigators to study phenotypic effects of modifying levels of expression of specific genes, either alone or in combination. Before RNAi was discovered, such studies were either not possible or were exceedingly difficult using human or mammalian cells of otherwise identical genetic backgrounds. We have studied phenotypic effects on chromosomal radiosensitivity and cell killing following the knock-down of DNAPKcs after transfection of normal human cells with small interfering RNA (siRNA). We have also studied effects and interactions on other proteins. Results of these and other experiments in the overall context of chromosomal radiosensitivity, as well as various applications of this technology for general studies in DNA damage processing, genome stability, mutagenesis, and cancer will be reviewed. [J Radiat Res 44:372 (2003)]

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In the Tokai-mura accident of September 1999, residents received not only gamma rays but also neutrons. For the estimation of the neutron doses, the quality factor proposed in ICRP 1977 Recommendation was used. Thereafter in October 2000, Japanese laws for radiation protection adopted the ICRP 1990 Recommendation, in which radiation-weighting factors were proposed for assessing stochastic effects of high LET radiation. However, for risk assessment, reexamination of the biological effects of low energy neutrons is considered. Although relative biological effectiveness (RBE) should be evaluated, it is hard to compile past data of experimental animals because of variations of experimental materials and methods in each experiment. It also needs to examine how to extrapolate the data from experimental animals to human.In this symposium, 1) suggestions from physical point of view, 2) present biological experiments in Japan, 3) problems for assessing neutron risks, will be presented, and then future researches and systems for promoting them will be discussed. [J Radiat Res 44:372-373 (2003)]

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Neutron, one of indirectly ionizing radiation, gives dose to substances in a very complicated manner. Dose deposition profile for neutrons depends significantly on the size of substance as well as incident energy. In the neutron dosimetry in radiation effect study, it is important to understand how neutrons transport in the material, what kind of secondary radiations or charged particles neutrons produce, and how these charged particles deposit their energy into the substance, in addition to the information of incident neutron energy. As an example, while recoiled protons give major absorbed dose in the incidence of neutrons above 100 keV, electrons due to gamma-rays produced by the capture reaction of hydrogen nucleus contribute to more than 90% of human absorbed dose in the incident of neutrons less than 10 keV. This means that the dose deposition profile for low-energy neutrons in the human body has a very similar aspect for gamma-ray exposure. It can be said from these facts that some detailed analysis of dose deposition profile by using computer simulation techniques should play an important role in biological effect study for neutron. [J Radiat Res 44:373 (2003)]

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Radiation weighting factor of low-energy neutron is an operational quantity inferred from the LET-RBE convention of charged particles and still remains highly conceptual. Currently, experimental data on chromosomal effectiveness of neutrons with different energy have been accumulated, including those of our filtered spectrum neutrons. The dose-response relationships of chromosome aberrations in the in vitro-irradiated human peripheral blood lymphocytes indicates that the quality factors are consistent with the those inferred from the LET-RBE convention for the monoenergetic neutrons in the energy range above 1 MeV, that is inversely proportional to neutron energy. However, there is little energy dependency for lower energy neutrons over a wide mean energy range down to 20 keV, their effective quality factors being stayed at high value similar to those of fission neutrons or thermal neutrons. This comes up to a serious problem that the effective quality factor or radiation weighting factor of low energy spectrum neutrons are not a simple sum of the currently proposed energy-dependent radiation weighting factors. A possible reasoning for the discrepancy will be discussed. [J Radiat Res 44:373 (2003)]

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This study was undertaken to investigate the tumorigenesis of monoenergetic neutron in mice. Monoenergitic neutron (HIRRAC) of 0.18, 0.32, 0.6 and 1.0 MeV were generated and irradiated in 6-weeks old both sexes B6C3F1 mice at dose of 50 cGy (0.5 cGy/min). The groups were observed for 13 months after irradiation. There were no significant differences of tumor inductions among energies.In another experiment, 7-weeks old C3H male mice were irradiated with 12.5, 25, 50 and 100 cGy of monoenergitic neutron of 0.2 and 0.6 MeV. Two weeks after irradiation, the male mice were mated with virgin 9-weeks old C57BL female and the mice shown an increased incidence of sperm abnormalities, which led to embryonic lethalities. Furthermore, liver tumors in male mice in 25 and 50 cGy of 0.6 MeV were tendency increased in contrast to unirradiated group. [J Radiat Res 44:373 (2003)]

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Biological effects of neutrons are larger than those of low-LET radiation and those depend on their energy. Since, neutron sources such as accelerator, reactor and cosmic-rays must be taken into consideration to assess human risk from neutrons, the researches on wide range of neutron energy is needed. The critical accident occurred at 1991 in Japan caused necessity of researchs on biological effects of neutrons. While many researches had been conducted to assess biological effects of neutrons, especially carcinogenesis in experimental animal, details of mechanisms of them are still obscure. Since 2001, NIRS has started the biological effects research program on neutrons to evaluate two major subjects: relative biological effects (RBE) of neutrons for carcinogenesis and for effects on developing nervous systems in rodents. In this program, to investigate energy dependency of biological effects of neutrons cyclotron-derived fast neutrons (10MeV) are used and electrostatic accelerator-derived neutrons (~2MeV) will be available in the near future. In this symposium, we will present recent results obtained in our laboratory, and also discuss our future plans. [J Radiat Res 44:373-374 (2003)]

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For low LET radiations, the cancer risk has been estimated mainly based on the epidemiological data of the atomic bomb survivors in Hiroshima and Nagasaki. However, the risk from neutrons cannot be directly estimated from human data since no epidemiological data is available. For the cancer risk from neutrons, the RBE of neutrons has been investigated based on experimental data by comparing with the dose response of gamma radiation. The risk estimate using such a method is influenced by uncertainty of risk estimates of gamma radiation in low dose region because the slope of the dose response curve from gamma irradiation decreases to zero. The most important issue in the neutron risk estimate is inverse dose-rate effects that show a reduced risk as dose rate increases. There are some evidence for inverse dose-rate effects in endpoints such as mutations and transformations, but mechanistic explanations are needed to estimate how carcinogenic effects are dependent upon dose and dose rate. We examined how mutagenic effects depending upon dose rate have an influence on multistage process in carcinogenesis. [J Radiat Res 44:374 (2003)]

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Telomeres are nucleoprotein structures that maintain genomic stability by protecting the ends of linear chromosomes. In striking contrast to natural chromosomal termini, broken chromosome ends produced by DNA double strand breaks (DSBs) are highly recombinogenic, and represent a major threat to the integrity of the cell's genome due to their potential for causing chromosomal rearrangements that contribute to genomic instability and tumorigenesis. We've demonstrated that effective end-capping of mammalian telomeres has a seemingly paradoxical requirement for proteins more commonly associated with DNA DSB repair. Ku70, Ku86, and DNA-PKcs all participate in DSB repair through non-homologous end-joining. Mutations in any of these genes cause spontaneous chromosomal end-to-end fusions that maintain large blocks of telomeric sequence at the points of fusion that are not a consequence of telomere shortening. We've also shown that nascent telomeres produced via leading-strand DNA synthesis are especially susceptible to these end-to-end fusions. Here we report that impaired end-capping also allows dysfunctional telomeres to misjoin to broken chromosome ends created by radiation-induced DSB. [J Radiat Res 44:374 (2003)]

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Carcinogenesis is a multistep process by which a normal cell gradually develops into a transformed malignant cell. The presence of structural and numerical chromosomal aberrations in tumour cells suggests that chromosomal instability (CIN) plays and important role in carcinogenesis. Numerous investigations have demonstrated that ionizing radiation is able to induce CIN. Research aimed to elucidate the precise role of ionizing radiation induced CIN in carcinogenesis requires methods capable to measure true CIN, i.e. the continuous formation of de novo chromosomal abnormalities. In a pilot study, we have successfully established a novel method to detect and quantify CIN within in situ fixated colonies of human epithelial cells. This strategy allows to visualize the occurrence of CIN within a colony (the progeny of a single cell) and to quantify the rate of CIN as events per number of cell generations. Preliminary results suggest that CIN initiated by telomere dysfunctioning, might be involved in the immortalization of these cells. More details of the colony based in situ fixation method will be presented and our preliminary results discussed. [J Radiat Res 44:374 (2003)]

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To know the mechanism for delayed formation of chromosome aberrations by radiation, we established the experimental system to analyze delayed chromosome aberrations using a microcell-mediated chromosome transfer. We investigated chromosome alterations by FISH in two different conditions. In one condition, an irradiated human chromosome was transferred into unirradiated recipient mouse cells. In the other condition, an unirradiated human chromosome was transferred into irradiated recipient mouse cells. The results indicated that the irradiated human chromosome was unstable in the unirradiated recipient cells to be rearranged with the recipient mouse chromosomes and that the unirradiated human chromosome also showed an unstable nature in the irradiated recipient cells. Telomere FISH analysis indicated that end-to-end fusions were involved in the formation of delayed chromosome aberrations. These findings suggest that delayed chromosome aberrations can be formed by the interaction between a damaged chromosome and an intact chromosome possibly mediated by telomeric instability. [J Radiat Res 44:374-375 (2003)]

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Chromosomal double strand breaks (DSBs) are usually repaired in mammalian cells through either of two pathways: end-joining (EJ) or homologous recombination (HR). To clarify the relative contribution of each pathway and the ensuring genetic changes, we developed a system to trace the fate of DSBs in the human genome by introducing restriction enzyme I-SceI site into thymidine kinase gene (TK) of human lymphoblastoid cell line (TK6). A DSB in the TK gene stimulated EJ as well as inter-chromosomal HR, but EJ contributed to the repair of DSBs over 100 times more frequently than HR. Molecular analysis revealed that EJ mainly causes small deletions limited to the TK gene. Seventy percent of the small deletion mutants analyzed showed 100 to 4,000 bp deletions with a 0 to 6-bp homology at the joint. Another 30%, however, were accompanied by complicated DNA rearrangements, presumably the result of sister chromatid fusion and breakage-fusion-bridge (BFB) cycle. BFB cycle could be an important mechanism for explaining delayed chromosomal instability caused by DSBs. HR, on the other hand, always resulted in non-crossing-over gene conversion. [J Radiat Res 44:375 (2003)]

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Radiation induced genomic instability is characterized by two features; untargeted and delayed mutation. We have shown that irradiation of sperm results in induction of maternal allele mutation at a minisatellite and the pink-eyed locus in F1 mice. Detailed analysis of embryos fertilized by irradiated sperm indicated that DNA synthesis of both male and female pronuclei is suppressed p53 dependently. This p53 dependent S checkpoint operates also in tissue culture cells. In the cells irradiated with less than 2.5 Gy, p53 aids ATM dependent phosphorylation of PCNA which then slows down the replication fork movement. Under this condition, PCNA forms foci in irradiated cells. In the absence of p53, PCNA was distributed in the nucleus homogeneously and DNA replication progresses at a rate equivalent to that of unirradiated cells. The relation between slowing-down of replication fork and recombination will be discussed. [J Radiat Res 44:375 (2003)]

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DNA double-strand break (DSB), which is often induced by ionizing radiation, is the most serious damage in genome. There are at least two pathways which can repair DSBs: non-homologous end-joining (NHEJ) and homologous recombination (HR). When DSBs are generated by radiation, ATM kinase, which is activated by auto-phosphorylation and dissociation of their homodimer., phosphorylates histone H2AX. Subsequently, many repair proteins are recruited to the DSB sites and they activates damage responding pathways. A key role protein, Nbs1, physically interacts with phospho-H2AX for recruitment of a multi-functional repair complex, Mre11/Rad50/Nbs1, to DSB sites. This physical interaction requires the fork-head associated (FHA) domain of Nbs1 protein and the complex was found to be essential for HR. In this presentation, we will discuss about the processing and signaling pathways responding to radiation-induced DSBs. [J Radiat Res 44:375 (2003)]

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It has been generally accepted that LDRE results from the SLD repair. As the dose rate is lowered and the treatment time protracted, more and more SLD can be repaired during the exposure. Recently we found that SLD repair due to DSB repair mediated by HR. To study the molecular mechanism of LDRE, we analyzed the knock-out mutants KU70^−/-, RAD54^−/-, and KU70^−/-/RAD54^−/- of the chicken B-cell line, DT40. Rad54 participates in the HR repair of DSBs, while Ku proteins are involved in NHEJ. Survival enhancement by LDR irradiation was observed in parent DT40 and RAD54^−/- cells but not in NHEJ deficient KU70^−/- and KU70^−/-/RAD54^−/- cells. In the LDRE, NHEJ pathway was more important than HR pathway. This suggests that LDRE are not directly attributable to the SLD repair because the SLD repair results from the HR pathway of DSBs. Under continuous LDR irradiation, dividing chicken cells can progress through the cell cycle. Since NHEJ-deficient cells will be killed in G₁ phase, NHEJ pathway plays an important role in LDRE. [J Radiat Res 44:375-376 (2003)]

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We have studied whether the p53-dependent apoptosis induced by acute radiation is interfered with pre-irradiation at a low dose or a low dose-rate in human cultured cells and whole body of mouse. In human cultured cells, we found that a challenge irradiation with X-ray immediately after chronic irradiation resulted in lower levels of p53 and p53-dependent apoptosis than those observed after the challenge irradiation alone. In mouse spleen, we found significant suppression of them induced by challenge irradiation at a high dose-rate when mice were pre-irradiated with a low dose or a low dose-rate irradiation. In addition, we did not find any radioadaptive response in DNA-PKcs deficient scid mice. These findings suggest that pre-irradiation at a low dose or a low dose-rate suppressed the p53-dependent apoptosis through the post-translational modification of target molecules by DNA-PK. We expect that the present findings will provide useful information in the health care of radiation workers and the general population. [J Radiat Res 44:376 (2003)]

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Normal function of the p53 gene is integral to the cellular response to genotoxic stress. In order to investigate the in vivo role of p53 in surveillance against mutation, and particularly to address the significance of p53-dependent apoptosis, we have used wild-type p53(+/+) and null p53(-/-) mice to determine the mutant frequency at the TCR locus following exposure to gamma-rays. The induced mutant frequencies at 3Gy were 15.6 x 10⁻⁴ and 33.2 x 10⁻⁴ for p53(+/+) and p53(-/-) mice, respectively. However, when the dose rate was reduced from 61 to 0.07 Gy/h, the mutant frequency at the TCR locus did not increase at all for p53(+/+) mice, whereas the dose of 3Gy remained mutagenic for p53(-/-) mice, which are unable to carry out p53-dependent apoptosis. These results indicate that p53 deficiency should lead to an increased mutant frequency by failed elimination of the mutagenic damage from the irradiated tissues. [J Radiat Res 44:376 (2003)]

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A total of 4000 SPF B6C3F1 mice were divided into four groups [three irradiated groups and one control group], each consisting of 500 male and 500 female mice. Irradiation was performed using ¹³⁷Cs gamma-rays at dose-rates of 20, 1 and 0.05 mGy/day with accumulated doses equivalent to 8000, 400 and 20 mGy, respectively. Partial results of pathological examination show that malignant lymphomas and soft tissue neoplasms at 20 mGy/day irradiated groups in both sexes appear to contribute to early deaths and consequent shorter life spans. The relationship between life shortening and non-neoplasm death however was not clear. The 20 mGy/day irradiated group appear to show a higher frequency of lung and endocrine neoplasm in females and Harderian gland neoplasms in both sexes. The experiment is currently in progress and is scheduled for completion in year 2004. This interim report is based on data collected from 1996 to the present. (The work is supported by grants from Aomori prefecture, Japan.) [J Radiat Res 44:376 (2003)]

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We have demonstrated that low dose-rate irradiation at around 1 mGy/hr suppressed the incidence of methylcholanthrene-induced skin tumor and radiation-induced thymic lymphoma in mice. We also found some of bio-protective functions, including anti-oxidative capacity and immune functions, were enhanced. To examine the possibility that the enhanced protective capacity may have some other effects in addition to the tumor suppression, we investigated the effects of low dose irradiation on disease model mice. In Type II diabetic C57BL/KsJ-db/db (db) mice the urine glucose level was improved in some of the mice irradiated at 0.70 mGy/hr, but not in non-irradiated control mice. In severe autoimmune MRL-lpr/lpr (lpr) mice immunological status was kept better in the mice irradiated at 0.35 or 1.2 mGy/hr. The incidence of a number of symptoms, including lymphadenopathy and proteinuria, was suppressed by the irradiation. For both of the strains, furthermore, the low dose-rate irradiation prolonged the life span of the irradiated mice.The studies on db mice and lpr mice were done by Takaharu Nomura and Yasuhiro Ina in our Research Center, respectively. [J Radiat Res 44:376-377 (2003)]

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In recent years, radiation biologists have clarified the biological response by radiation about mechanisms of DNA damage recognition, DNA repair, signal transduction, cell cycle, cell death and etc. We have searched breakthrough for radio-cancer therapy based on the knowledge of radiation biology. The wild-type p53 gene but not mutation and deletion of p53 gene efficiently induced apoptosis by radiation. To overcome this problem, we propose a novel p53-targeting radio-cancer therapy for mutant p53 (mp53) patients with chemical chaperone (glycerol) or molecular chaperone (p53 C-terminal peptide). These strategies are based on the conformation change of mp53 protein to wtp53 protein by glycerol or p53 C-terminal peptide. In addition, we propose a combination with gene therapy of wild-type p53 (wtp53) against p53-null cells. These p53-targeted tools for enhancement of apoptosis induction might be useful for radio-cancer therapy. Here, we want to discuss the effective cancer therapy by application of advanced radiation biology. [J Radiat Res 44:377 (2003)]

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Extensive studies performed in the last 10 years have unveiled a considerable amount of the molecular basis of apoptosis. Mitochondrial membrane permeabilization is one of the most critical events in apoptosis in mammals, because it leads to the release of apoptogenic factors, including cytochrome c, into the cytoplasm, which activates death-executing programs including caspases. The Bcl-2 family of proteins, consisting of anti-apoptotic and pro-apoptotic members, directly controls mitochondrial membrane permeability. Pro-apoptotic members of the family participate in sensing/transmitting apoptotic signals to the mitochondria, as well as permeabilization of mitochondiral membrane. We have been studying the molecular basis of function of Bcl-2 family proteins, as well as various aspects of apoptotic signaling and execution. In this symposium, I will focus particularly on the signaling pathway of DNA double strand break-induced apoptosis. We have been attempting to identify a molecule, which appears in the cytoplasm upon DNA double strand breaks and has a cytochrome c-releasing activity. By introducing our recent data, I will discuss how DNA double strand breaks trigger apoptotic signals, which are transmitted to the mitochondria and induce membrane permeabilization. [J Radiat Res 44:377 (2003)]

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Cu-diacetyl-bis(N-methylthiosemicarbazone) (Cu-ATSM) is a neutral divalent Cu-complex with high lipophylicity anf small morecular size. Cu-ATSM easily penetrate the cell membrane including blood-brain barieer, and can be reduced to monovalent Cu only in abnormally reduced conditions such as hypoxia. Using this characteristic, Cu-ATSM could be used for visualizing hypoxic tumors. The intratumoral accumulation of Cu-ATSM was different from that of F-18-fluorodeoxyglucose.The hypoxic tumor selectivity of Cu-ATSM is considered to be useful for the delivery system of therapeutic radionuclide to intratumoral ratdiotherapy. Cu-64 is a beta-emitting radinulide with half life of 13 hours. It could be produced using a ultra-small cyclotron by Ni-64(p, n)Cu-64 reaction. Using Cu-64-ATSM, cell toxicity as well as therapeutic ability was clarified. [J Radiat Res 44:377 (2003)]

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The ideal radiotherapy in 20th century is to deliver more doses to cancer region as confined as possible. This has been proved to be true by the success of brachytherapy. Recent advance of accelerator, computer and medical imaging have enabled this idea even by external x-ray beam. 3D-radiotherapy, intensity modified radiotherapy (IMRT) and heavy charged particle radiotherapy are example. However, this idea is not universally true. It may be true if the cancer arises in parallel organs, but not if the cancer is in serial organs. The more universal idea that must be adopted in 21st century is to deliver more doses to cancer cells as confined as possible. α particle and Li nucleus that are emitted by ¹⁰B(n, α)⁷Li reaction have very short track and high LET character. Therefore, if ¹⁰B compound accumulates in cancer cells selectively, only cancer cells are destroyed. Malignant glioma and melanoma are successfully treated by this boron neutron capture therapy. Advanced recurrent head and neck cancers also dramatically shrank without significant skin reaction. [J Radiat Res 44:377-378 (2003)]

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In March 1954, a thermonuclear test explosion was performed at Bikini Atoll of the Pacific Ocean and 23 Japanese fishermen were accidentally exposed to radiation from the fallout (powder of destroyed atoll with fission products). Contamination of the body surface with radioactive fallout caused beta-ray burns. They were also irradiated with gamma-ray from the fallout deposited on the deck and in the cabins. Internal contamination occurred through inhalation, ingestion, or wounds and also through food and water on the boat. Thus, this exposure caused combined radiation injuries including acute radiation syndrome (ARS), local burns, and internal contamination. The dose estimation of whole body was based on analysis of the fallout and interviews with fishermen. The estimated dose to whole body was from 170 to 700 rad during 14 days, a half or more of the dose was irradiated on the first day of the explosion. Whereas they developed the prodromal signs of ARS such as vomiting, the duration of exposure was relatively long and their clinical courses were slightly different from those of acute radiation exposure. [J Radiat Res 44:378 (2003)]

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The atomic bomb was dropped in 1945 Hiroshima and Nagasaki, the environmental radiation measurement by fallout was performed. By suffering calamity of 5th-Fukuryu-Maru by the H-bomb test of the March 1st 1954 Bikini Atoll, it became the time when the environmental radioactive contamination by the nuclear bombs in the atmosphere by the U.S.A. and old Soviet Union had been taken up greatly. The following contents are introduced about the flow of the times. 1. The measurement fallout effects in Hiroshima and Nagasaki with NEHER type ionization chamber. 2. A marine radiation measurement by the scintillation instruments according to Shyunkotu-Maru expedition in relation to a Bikini incident. 3. Environmental radioactive contamination that had not been noticed during 1945 to 1954. 4. Effect of the atmosphere nuclear explosion tests which are each of the USA and Soviet Union. 5. Effect of the greatest in our country by the 5th Chinas nuclear test in 1966. 6. Influence investigation of the Chernobyl accident acquired by national investigation. 7. The goal of investigation research of environmental radioactivity. [J Radiat Res 44:378 (2003)]

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Resettlement Program of Rongelap Island in Rongelap Atoll of Marshall Islands has been started since July 1998. Radiological investigation and its information will be urgently important for the people of Rongelap. The Rongelap Atoll was severely contaminated by radiological fallout due to the USA nuclear test of 15Mt March 1 1954. The 64 persons, who were evacuated by plane and boat from the island March 3, got 1.9 Gy for whole body. The Atomic Energy Committee of USA approved the return of the people of Rongelap to their atoll in February 1957. Two hundred and fifty people were returned to Rongelap Island on 29 June of the year. However in May 1985 they were reevacuated by their own will as a result of their fear of the radioactive contamination of Rongelap described in the 1982 DOE report of the northern Marshall Islands radiological survey. Rongelap Island were investigated on July 6-12 1999. Portable whole-body counting of Cs-137 was also carried out for workers. The present investigation finds that remarkable risk dose not exist in Rongelap Island from the radiation protection point of view. [J Radiat Res 44:378 (2003)]

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During the 1990s, neither atmospheric nuclear test has been conducted nor the severe nuclear accident has occurred, which resulted in no severe contamination in the atmosphere. Therefore, the current atmospheric radioactivity levels became extremely low, giving rise to insignificant public exposure. However, long-term monitoring of anthropogenic radioactivity in atmospheric deposition seems still important in terms of the environmental process study. In fact, the monitoring has revealed the process, so-called resuspension. In order to investigate the resuspension, ¹³⁷Cs/ ⁹⁰Sr activity ratios in the deposition were compared with those in surface soil samples. It was found that the ¹³⁷Cs/ ⁹⁰Sr ratio in the deposition samples at the MRI, Japan during the 1990s (average: 2.1) was not close to that of the Japanese surface soils (average: 4.5-7), which had been considered as the primary source. The findings suggest that the current radioactivity deposition is not composed of a single local component but a mixture of local and remote resuspension sources. This further lead to our noble hypothesis that large scale aeolian dust may play an important role as a remote source for the resuspension. [J Radiat Res 44:378-379 (2003)]

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Substantial amounts of plutonium have been delivered to the surface of the Pacific Ocean as a consequence of global fallout from atmospheric tests of nuclear weapons, which took place mostly during the 1950's and early 1960's. The second and significant input of plutonium to the Pacific Ocean was derived from tropospheric close-in fallout from nuclear weapons test at Bikini and Enewetak Atolls, Marshall Islands. In this symposium, I will present an overview of the distribution and behavior of plutonium in the western North Pacific Ocean, our new results of sediment trap experiments, and the future plan for material cycle studies in the ocean. [J Radiat Res 44:379 (2003)]

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We have provided evidence that long lived radicals (LLRs), produced by ionizing radiation, are highly mutagenic and transforming in mammalian cells. LLRs are effectively scavenged by vitamin C or by epigallocatechin-3-O-gallate (EGCG). LLRs are not involved in lethality or induction of chromosome aberrations. ESR spectra of LLRs produced in irradiated Syrian hamster embryo (SHE) cells were precisely analyzed. We now report results of experiments that define the relative amounts of LLR in DNA and proteins and identify the major protein radical as sulfinyl radicals (R-CH₂-S-O). LLRs yields of 99.8% are produced in proteins. We also identified a new type of LLR as H-added phenylalanine radicals. While our evidence does not rule out the possibility of important biological consequences of low-level, LLRs created by radiation in molecules besides proteins, it implicates protein radicals as playing a key role in genetic effects of ionizing radiation. We suggest that these novel radicals, wherever they reside, need to be considered in explanations of biological sequela of radiation. [J Radiat Res 44:379 (2003)]

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Many researcher studying in area of radiation biology have been believed that active short life-time radicals such as OH and H radicals, play an important role to express genotoxic effects of radiations in cells,such as mutation and cancer induction. However, in 1993 we found a new type ofradicals with long life-time(T1/2 is over 20hr) in gamma ray irradiated golden hamster embryo (GHE) cells at room temperature by using ESR spectroscopy. When vitamin C is added to the gamma- or X-irradiated cells at 20 min or 6 hr after the irradiation, respectively, vitamin C scavenge LLRsimultaneously with the drastic suppression of genotoxicity such as mutation and transformation.Addition of vitamin C to the cells before or after irradiation does not have any effects onreducing cell death and chromosomal aberration. Since reactive oxygen species (ROS) disappearwithin microsecond after the irradiation,vitamin C does not scavenge the ROS but LLR.Therefore,we have proposed that LLR must be responsible radicals for inducing mutation, and probablyimportant for the genotoxicity in the irradiated mammalian cells. [J Radiat Res 44:379 (2003)]

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Watanabe, Kumagai, Miyazaki and colleagues produced strong evidence that ionizing radiations induce new kinds of long-lived radicals (LLR) with half lives of minutes to hours in cellular proteins [Rad Res 160: 95, 2003]. LLR are not lethal but are transforming, and mutagenic. They are not scavenged by DMSO but are by vitamin C, EGC and RibCys {epigallocatechin-s-O-gallate and [2(R, S)-D-ribo-1', 2', 3', 4', - Tetrahydroxybutly]-thiazolidene-4-ca riboxylic acid}, respectively}. We find that vitamin C and RibCys significantly decrease yields of CD59⁻ mutants in human-CHO hybrid A_L cells exposed to high LET carbon ion radiation [290 MeV/nucleon, LET = 100 KeV/µmeters] and alter the mutational spectrum, even when added after radiation. The principal change in spectrum is reduction in prevalence of deletions of sizes detectable at the HPRT locus (<3Mbp) and of mutants displaying TGI. Thus LLR in cellular proteins may play an important role in triggering genomic instability, an effect reducible by post treatment with certain antioxidants. Supported by: Japanese Sci. Tech Agency, NIH-NCI RO1CA82309, NASANSCORT W19133. [J Radiat Res 44:379 (2003)]

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Any of physical, chemical or biological stressors can induce metallothionein (MT) synthesis in animals. A striking resistance to lethal damage from a 6-8 Gy radiation has been found in mice received various stressful pretreatments to induce MT in liver prior to irradiation.In the livers of the mice subjected to these pretreatments (e.g.injection of MnCl₂ 20mg Mn/kg or dermal excision of 2x2 cm²etc.), MT synthesis increased 5-7 fold (Matsubara et al. Radiat. Res. 1987).Firstly we confirmed that MT can act as a substitute of glutathione in NADPH-glutathione-reductase system in vitro. Secondly we measured the levels of organic radicals in the livers of the pretreated mice(Miyazaki et al.Radiat.Phys.Chem.1996). Since MT is a cystein-rich protein it can be a radical scavenger.It was found that the increased level of MT accelerates the scavenging organic radicals, having a half-life of about 10 hrs in the control and 1.5-3hrs in the pretreated ones so that gross levels of the radicals are kept constant in the liver even at the load of various stressors to the body. [J Radiat Res 44:380 (2003)]

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Non-reparable DNA double strand breaks (dsb) have been attributed to cellular effects induced by ionizing radiation. It is mentioned that radiation damages including dsb are nonspecific in chemical form and in sequence of bases. Recent findings, however, are that (1)5'G of 5'-GG-3' has the lowest ionization potential, indicating an efficient electron donor (2) hole migration exists to 5'G of 5'-GG-3' from neighboring ionized bases, (3)193 nm light induces strand breaks preferentially at G, possibly the hole migration intervening. Little is known the biological reason why the damage or dsb does occur preferentially at G. Structural biology consists of three fields, molecular biology, structural chemistry and computational chemistry. Molecular biology finds out biological function in terms of entity (molecule), and structural chemistry studies the biological function in terms of structure of the molecule using X-ray crystallography and NMR spectroscopy. The computational chemistry studies the biological functions in terms of dynamic properties of the molecule. As an approach of the computational chemistry we exemplify the dynamic properties of the DNA containing a ssb at 5'G 0f 5'-GG-3' using the molecular dynamics simulation. [J Radiat Res 44:380 (2003)]

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Clustered DNA damage has been suggested be specific to ionizing radiation. Such damage is considered to be formed by localized energy deposition by radiation and difficult to be repaired. Therefore, the initial physical feature of ionizing radiation is an important determinant biological consequences following radiation exposure. Monte Carlo simulation of track structure could provide the details of the energy deposition distribution in nanometer scale, which is closely correlated with the initial conditions of DNA damage. Spectrum and spatial distribution of DNA damage and its correlation with biological consequences are studied by modelling and simulation of both direct and indirect actions. Higher-order structure of DNA model described in atomistic revel has been also recently developed to mimic cellular condition. This paper presents contribution and possible role of modelling of track structure, DNA damage and biological consequences to understand the mechanism of radiation biological effect. [J Radiat Res 44:380 (2003)]

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Exploring electronic states of DNA is essential to understand the interaction between the molecule and charged particles in a track of ionizing radiation. Photoabsorption cross section of DNA, which is strongly involved in oscillator strength distribution, has been investigated because the cross section should reflect the electronic and excitation states of DNA. On the other hand, it has been reported that a hole created on DNA by radiation could migrate to a guanine site and induce an oxidative base lesion such as 8-oxo-G. Localization of the lesion at guanine sites can be interpreted as an effect of its relatively lowest ionization potential value (oxidation trend; G>A>C>T). Recent results obtained from spectroscopic studies and theoretical calculations on the electronic states of DNA will be presented. These newly introduced methods are becoming powerful techniques to reveal the mechanism of DNA damage and damage repair process by enzymes. [J Radiat Res 44:380-381 (2003)]

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It is well known that reactive oxygen species, UV and radiation can induce sequence-specific DNA damage. We have investigated sequence specificity of oxidative stress-mediated DNA damage by using ³²P-labeled DNA fragments (human c-Ha-ras-1, p16, p53 genes and telomeric oligonucleotide). Free hydroxyl radical and peroxynitrite cause DNA damage with no marked site specificity. Singlet oxygen (¹O₂)-mediated DNA damage is caused at every guanine. Furthermore, sulfate radicals, nitrogen-centered radicals and oxygen-centered radicals show different sequence specificity. UVA radiation also causes DNA damage at the 5'-G in GG through electron transfer in the presence of certain photosensitizers. This guanine is easily oxidized because a large part of the highest occupied molecular orbital is distributed on this site. On the basis of these findings, the sequence specificity of DNA damage is presumably determined by (a) redox potential of reactive species; (b) ionization potential of DNA bases; (c) site-specific binding of metal ion to DNA. Here we discuss the mechanisms of sequence-specific DNA damage in relation to carcinogenesis and aging. [J Radiat Res 44:381 (2003)]

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Compaction of DNA is a common feature in native genomes. The manner of packaging is expected to play an essential role in the biological functions of DNA, such as replication and transcription. We have studied the conformational change of long duplex DNA molecules through single molecular chain observation using fluorescence microscopy. It has been found that individual DNA molecules undergo large discrete transition between elongated coil and folded compact states. We have examined the effect of various chemical species on the higher order structure of giant DNA molecules. It has been shown that DNA molecules take rich variety of different morphologies, including intra-chain segregation, pearling structure, and spool like structure and that a strong correlation was found between the morphology of DNA and the sensitivity to restriction enzyme activities. It has also been found that on/off change in the transcriptional activity is induced accompanied by the transition of higher order structure on DNA. It is expected that the application of single chain observation will be useful to shed light on the mechanism of radiation damage on DNA molecules. [J Radiat Res 44:381 (2003)]

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We have developed an AFLP-based gene expression profiling method called High Coverage Expression Profiling (HiCEP) analysis. Improvements on the selective PCR technique we have reduced the rate of false-positive peaks to approximately 2% and consequently the number of peaks, including overlapping peaks, has been markedly decreased. The low false-positive rate enables us to analyze gene expression with wide coverage by means of 4-nucleotide recognition restriction enzymes for fingerprinting mRNAs. The method detects 70-80% of all transcripts, including non-coding transcripts, unknown and known genes. We can determine the relationship between peaks and original transcripts unequivocally. This will make it practical to prepare a database of all peaks, allowing gene assignment without having to isolate individual peaks. The procedure is highly reproducible and sensitive enough to detect even a 1.2-fold difference in gene expression. The method requires no sequence information and so is applicable even to eukaryotes for which there is no genome information available. [J Radiat Res 44:381 (2003)]

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RNA interference(RNAi) is an evolutionarily conserved mechanism that responds to double-stranded RNA(dsRNA) by sequence-specific silencing of homologous genes. RNAi has been used as a reverse genetic tool to study gene function in multiple model organisms, including Caenorhabditis elegans and Drosophila. However, one obstacle to achieving RNAi in mammal cells is that dsRNAs longer than 30nt will activate an antiviral response, leading to the cell death. This obstacle has been recently overcome by Elbashir et al who found that RNAi in mammalian cells can be achieved by chemically synthesized short interfering RNA(siRNA) that are 21nt in length, short enough to evade the host interferon response. Therefore, now this technique can be broadly used for analysis of mammalian gene functions. Furthermore, DNA vector-based approach has been also developed. We will report a practical and theoretical update on our and others approaches to silencing mammalian genes, and discuss the possible application of this new technology. [J Radiat Res 44:381-382 (2003)]

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RNAi is a process to knock down the expression of a specific gene by injecting double stranded RNA and first described in C. Elegance and other organisms. Recently, the application of this technique was extended to mammalian systems by introducing short interfering RNA (siRNA) which consists of double stranded 21 nucleotide RNA with two nucleotide 3'overhangs. In order to apply RNAi to radiation biology, we have succeeded in silencing a NHEJ related DNA-PKcs gene in normal human fibroblasts. As a result, normal cells were changed to radiosensitive cells by reducing the degree of DNA double strand break (DSB) repair (Peng et al 2002). We also have tired to knock down another NHEJ related gene, Ligase IV by using Hemagglutinating virus of Japan envelop (HVJ-E) and a partial success was obtained by increasing the radiosensitivty of normal cells. These results indicate that a strategy of transiently silencing a DSB repair gene may be useful in radiation therapy. [J Radiat Res 44:382 (2003)]

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The Rad52 protein plays important roles in the homologous recombinational repair (HRR) of double strand breaks of chromosomal DNA. In this study, we found that the human Rad52 protein catalyzed homologous pairing, which is an essential step for the HRR pathway. The N-terminal domain of Rad52 was identified as the homologous-pairing domain by a protease mapping experiment, and we determined the crystal structure of this homologous-pairing domain at 2.85 angstrom resolution, which revealed that the eleven monomers tightly associate into a ring. Surface potential analysis revealed that the positively charged groove encircles the Rad52 ring and contains well-conserved amino acid residues. Among the residues, those essential for ssDNA and dsDNA binding were actually identified by a mutational analysis. Thus, Rad52 is likely to bind DNA outside the undecameric ring. Furthermore, the structure of an ssDNA bound to Rad52 was determined by NMR spectroscopy, and was found to be extended about 1.5 times relative to the B-form DNA, which is similar to that bound to the bacterial homologous-pairing protein, RecA. [J Radiat Res 44:382 (2003)]

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The homochirality of biological amino acids (L-amino acids) or the RNA or DNA backbone ribose (D-sugars) might be established before the origin of life. It has been considered that D-amino acids and L-sugars were eliminated on the primitive earth. Therefore, the presence and function of D-amino acids in living organism have not been studied. However, we have previously shown that Asp-151 and Asp-58 residues invert to the D-beta-isomers at a high degree in alpha A-crystallin from the human eye lens during aging. These modification can cause major changes in structure, since different side chain orientations can induce an abnormal peptide backbone. Similar reactions were also reported in beta-amyloid protein of Alzheimer disease. We suggests that UV irradiation is also closely related to the formation of D-beta-Asp in the protein of lens and skin from elderly person. We propose why racemization/isomerization occurs at specific sites in proteins. [J Radiat Res 44:382 (2003)]

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There has been observed the difference between measured neutron activation data and DS86 calculation. The measured data were lower than DS86 at the short range and higher more than 800m ground range. The collaboration between US and Japan WGs began in 1994 and finished in 2003. The new AMS technique has been developed to measure neutron activation of Cl-36 and Ni-63. At the end of the 2001 we decided to perform intercomparison study between Eu-152 and Cl-36 measurements to solve the discrepancy between the measurement and DS86. The 9 exposed samples were selected for intercomparison of the Eu-152 and Cl-36 measurements. Eu-152 was measured by the Komura's group of Kanazawa University. Cl-36 was measured at three laboratories: Nagashima's group at University of Tsukuba, Straume's group University of Utah and Ruehm's group at Technical University of Munich. As the result of the intercomparison study, the Eu-152 and Cl-36 data each other agreed well within 1.2km and also the data agreed with DS02. [J Radiat Res 44:382-383 (2003)]

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