Journal of Radiation Research
Online ISSN : 1349-9157
Print ISSN : 0449-3060
Volume 49, Issue 6
Displaying 1-11 of 11 articles from this issue
Regular Papers
  • Natacha BERNARD, Antonio J. ALBERDI, Marie-Laure TANGUY, Henri BRUGERE ...
    2008 Volume 49 Issue 6 Pages 565-577
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: October 04, 2008
    JOURNAL FREE ACCESS
    To answer the still unresolved question of the possible leukemogenic effects of extremely low frequency magnetic fields (ELF-MFs) and of their harmonics on the incidence of B acute lymphoblastic leukemia in children, we used an animal model to explore the possible co-initiating or co-promoting effects of ELF-MFs on the development of leukemia. We used a rat model in which B acute lymphoblastic leukemia is chemically induced by a nitrosurea derivative. From the onset of the chemical treatment, the animals were also exposed to ELF-MFs (100 μT, sinusoidal 50 Hz MFs), with or without harmonics. The experiment was conducted on 280 rats. We compared body weight and survival time, percentage of bone marrow blast cells, cumulative incidence of leukemia and type of leukemia in the unexposed groups and in the groups exposed to 50 Hz MFs, with and without harmonics. The results showed no significant differences between exposed and unexposed rats for any of these parameters (p > 0.05). Significant changes in the leukemia type obtained after γ-irradiation of the leukemia model, showed its sensitivity to a physical agent. Our results do not support the hypothesis that ELF-MFs, with or without harmonics, affect the development of B acute lymphoblastic leukemia in children.
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  • Dusan SOKOLOVIC, Boris DJINDJIC, Jelenka NIKOLIC, Gordana BJELAKOVIC, ...
    2008 Volume 49 Issue 6 Pages 579-586
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: September 29, 2008
    JOURNAL FREE ACCESS
    Purpose: The aim of the study was to evaluate the intensity of oxidative stress in the brain of animals chronically exposed to mobile phones and potential protective effects of melatonin in reducing oxidative stress and brain injury. Materials and methods: Experiments were performed on Wistar rats exposed to microwave radiation during 20, 40 and 60 days. Four groups were formed: I group (control)- animals treated by saline, intraperitoneally (i.p.) applied daily during follow up, II group (Mel)- rats treated daily with melatonin (2 mg kg-1 body weight i.p.), III group (MWs)- microwave exposed rats, IV group (MWs + Mel)- MWs exposed rats treated with melatonin (2 mg kg-1 body weight i.p.). The microwave radiation was produced by a mobile test phone (SAR = 0.043-0.135 W/kg). Results: A significant increase in the brain tissue malondialdehyde (MDA) and carbonyl group concentration was registered during exposure. Decreased activity of catalase (CAT) and increased activity of xanthine oxidase (XO) remained after 40 and 60 days of exposure to mobile phones. Melatonin treatment significantly prevented the increase in the MDA content and XO activity in the brain tissue after 40 days of exposure while it was unable to prevent the decrease of CAT activity and increase of carbonyl group contents. Conclusion: We demonstrated two important findings; that mobile phones caused oxidative damage biochemically by increasing the levels of MDA, carbonyl groups, XO activity and decreasing CAT activity; and that treatment with the melatonin significantly prevented oxidative damage in the brain.
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  • Bo ZHANG, Meng WANG, Yuan YANG, Yan WANG, Xueli PANG, Yongping SU, Jun ...
    2008 Volume 49 Issue 6 Pages 587-596
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: September 19, 2008
    JOURNAL FREE ACCESS
    ERp29 is a resident protein of the endoplasmic reticulum (ER) lumen, which is thought to be involved in the folding of secretory proteins. In our previous work, it was found that, when treated with ionizing radiation (IR), the ERp29 expression was increased in mouse intestinal epithelia and cultured IEC-6 cells, which suggested that ERp29 might be a radiation-induced gene. The current work is to confirm the induction of ERp29 by IR and to analyze its role in irradiated IEC-6 cells. Our results showed that ERp29 expression was elevated by IR in IEC-6 cells at mRNA and protein levels in a time-dependent manner. IEC-6 cells with different exogenous ERp29 expression were obtained by transfection with sense and antisense expression vectors of ERp29 coding region. As ERp29 expression was inhibited, these cells exhibited more serious radiation injury and more sensitivity to IR-induced apoptosis. To further elucidate the induction of ERp29, we analyzed the XBP1 expression after IR. Results showed that the spliced form of XBP1 mRNA rapidly reached a peak at 3 hours after irradiation, which indicated that UPR sensor was involved in radiation and might be a reason to induce ERp29 expression. Our results demonstrate that ERp29 is a radiation associated protein and plays an important role in protecting cells from IR.
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  • Mauro BELLI, Daniela BETTEGA, Paola CALZOLARI, Roberto CHERUBINI, Giac ...
    2008 Volume 49 Issue 6 Pages 597-607
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: November 06, 2008
    JOURNAL FREE ACCESS
    This work aimed at measuring cell-killing effectiveness of monoenergetic and Spread-Out Bragg Peak (SOBP) carbon-ion beams in normal and tumour cells with different radiation sensitivity. Clonogenic survival was assayed in normal and tumour human cell lines exhibiting different radiosensitivity to X- or γ-rays following exposure to monoenergetic carbon-ion beams (incident LET 13-303 keV/μm) and at various positions along the ionization curve of a therapeutic carbon-ion beam, corresponding to three dose-averaged LET (LETd) values (40, 50 and 75 keV/μm). Chinese hamster V79 cells were also used. Carbon-ion effectiveness for cell inactivation generally increased with LET for monoenergetic beams, with the largest gain in cell-killing obtained in the cells most radioresistant to X- or γ-rays. Such an increased effectiveness in cells less responsive to low LET radiation was found also for SOBP irradiation, but the latter was less effective compared with monoenergetic ion beams of the same LET. Our data show the superior effectiveness for cell-killing exhibited by carbon-ion beams compared to lower LET radiation, particularly in tumour cells radioresistant to X- or γ-rays, hence the advantage of using such beams in radiotherapy. The observed lower effectiveness of SOBP irradiation compared to monoenergetic carbon beam irradiation argues against the radiobiological equivalence between dose-averaged LET in a point in the SOBP and the corresponding monoenergetic beams.
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  • Haiying FU, Yosuke KATSUMURA, Mingzhang LIN, Kuniki HATA, Yusa MUROYA, ...
    2008 Volume 49 Issue 6 Pages 609-614
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: November 06, 2008
    JOURNAL FREE ACCESS
    The repair activities of silybin (SLB) and its analogues towards the oxidizing deoxyguanosine monophosphate (dGMP) hydroxyl radical adducts are investigated by pulse radiolytic techniques. On pulse irradiation of nitrous oxide saturated 2.0 mM dGMP aqueous solution containing 0.1 mM silybin at neutral pH, the transient absorption spectrum of the dGMP hydroxyl radical adducts decreases with the formation of the phenoxyl radical of silybin within tens of microseconds, indicating that there is a repair reaction between the dGMP hydroxyl radical adduct and silybin. The rate constant of the repair reaction is calculated to be 1.0 × 109 M-1s-1 for silybin. The repair activity of hesperetin (HESP), naringin (NAN) and naringenin (NAR) towards hydroxyl radical adducts of dGMP are also studied.
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  • Lalla Rajaa RHENIMI, Naglaa Fathi ABU-NASR, Kazuo YAMAMOTO
    2008 Volume 49 Issue 6 Pages 615-622
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: September 06, 2008
    JOURNAL FREE ACCESS
    Nitropyrene, a mutagenic and carcinogenic component of diesel exhaust, has been shown to be a potent bacterial and mammalian mutagen. There is, however, some controversy regarding the genotoxic effects of 1-nitropyrene towards yeast. To obtain insights into the mechanisms of 1-nitropyrene-induced mutations in Saccharomyces cerevisiae, we have attempted to characterize the genetic alterations that inactivate the endogenous CAN1 gene either in haploid cells or in heterozygous diploid cells. 1-Nitropyrene, without any activation treatment, showed a substantial toxic effect until 500 μM. The mutation frequency in haploid cells treated with 500 μM of 1-nitropyrene was 1.59 × 10-5, which is 15-fold higher than the control value. Sequencing of mutants indicated that both frameshifts and base substitutions were increased. In diploid cells treated with 500 μM of 1-nitropyrene, the frequency with which can1Δ::LEU2/can1Δ::LEU2 was converted from CAN1/can1Δ::LEU2, a phenotypic change from a canavanine-sensitive to canavanine-resistant form, was 8.59 × 10-4, which is 9.15-fold higher than the spontaneous level. More than 99% of the 1-nitropyrene-induced mutations in canavanine-resistant diploid cells constituted a gene conversion or crossover. Chromosome loss was not increased after treatment with 1-nitropyrene. These results suggest that 1-nitropyrene is an agent that efficiently induces point mutations, gene conversion, and crossover, but not chromosome loss, in S. cerevisiae.
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  • Shunsaku SASAKI, Nobuo FUKUDA
    2008 Volume 49 Issue 6 Pages 623-633
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: October 29, 2008
    JOURNAL FREE ACCESS
    Female B6C3F1 mice were irradiated at day 17 prenatal period, day 0, 7, 35, 105, 240, 365 and 550 postnatal period with doses of 0.10 to 5.70 Gy gamma rays from 137Cs. All mice were allowed to live through their entire life spans under a specific-pathogen free condition. The excess relative risk for prevalence at the time of death of ovarian tumors was used as a comprehensive measure of radiation effect. The excess relative risks at 1 Gy were estimated for all irradiated groups based on the dose-response relationships and compared to each other. A marked increase in susceptibility was found during the age between day 17 prenatal and day 0 postnatal period. A drastic decrease in susceptibility was observed during the period between day 105 and day 240. The shape of the dose-response curve was downward concave in mice irradiated at day 0, 7, 35 or 105 postnatal period, whereas, the downward curvature of dose-response was not observed in mice irradiated at day 17 prenatal period, day 240, 365 or 550 postnatal period. It has become obvious that mice of the early postnatal, pre-puberty and young adult periods are highly susceptible to induction of ovarian tumors by gamma rays.
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  • Yukio NIIMURA, Toshiko MOUE, Nobuyoshi TAKAHASHI, Ken-ichi NAGAI
    2008 Volume 49 Issue 6 Pages 635-644
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: November 06, 2008
    JOURNAL FREE ACCESS
    When M10 cells derived from mouse lymph nodes were irradiated with the UVB lamp at a peak emission of 312 nm, the cell growth was suppressed in proportion to irradiation time (10-30 s) and cell apoptosis was also induced by the irradiation. Dynamic changes in 597 genes after exposing these cells to UVB irradiation were investigated by DNA array analysis using array membranes and a 33P-labeling probe. After 2 h of irradiation, the gene expression in the cells was examined and compared with that in untreated cells. Radioactivity was analyzed using Array Gauge software. The data were further processed using software, EX-ARRAY, which was developed for extracting significant data from the results of 2 background-subtraction methods, i.e., global and local background subtraction. The number of genes suppressed under UV irradiation increased with irradiation time, while that of activated genes decreased. Finally, we confirmed 4 genes (HMG-14, CDX-2, MCP-3, and GRP-78) to be up-regulated and confirmed their activation by northern blot. We propose these genes as the new biomarkers of lymphocyte sensitive to UVB irradiation.
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  • Akihisa TAKAHASHI, Nobuhiro YAMAKAWA, Tadaaki KIRITA, Katsunori OMORI, ...
    2008 Volume 49 Issue 6 Pages 645-652
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: November 06, 2008
    JOURNAL FREE ACCESS
    To identify the repair dynamics involved in high linear energy transfer (LET) radiation-induced DNA damage, phospho-H2AX (γH2AX) foci formation was analyzed after cellular exposure to iron ions (Fe-ions, 500 MeV u-1, 200 KeV μm-1). The foci located at DNA damage sites were visualized using immunocytochemical methods. Since H2AX is phosphorylated at sites of radiation-induced double strand breaks (DSB), γH2AX foci were used to detect or illuminate tracks formed by DSB after exposure to various doses of ionizing radiation. Additional DSB-recognition proteins such as ATM phospho-serine 1981, DNA-PKcs phospho-threonine 2609, NBS1 phospho-serine 343 and CHK2 phospho-threonine 68 all co-localized with γH2AX at high LET radiation induced DSB. In addition, Fe-ion induced foci remained for longer times than X-radiation induced foci. These findings suggest that Fe-ion induced damage is repaired more slowly than X-radiation induced damage, possibly because Fe-ion induced damage or lesions are more complex or extensive. Antibodies for all these phosphorylated DNA DSB recognition proteins appear to be very effective for the detection and localization of DSB.
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  • Da-Hee JEONG, Moon-Jung GOO, Il-Hwa HONG, Hai-Jie YANG, Mi-Ran KI, Sun ...
    2008 Volume 49 Issue 6 Pages 653-660
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: November 12, 2008
    JOURNAL FREE ACCESS
    Apoptosis occurs early after irradiation and may be a good indicator of radiation damages. Since elevated levels of TGF-β are associated with radiation-induced inflammation, the null mice of Smad3, a key downstream mediator of TGF-β, show accelerated healing of irradiated injury. In order to evaluate resistance to radiation-induced liver injuries in Smad3-null mice, we determined the occurrence of apoptosis and the expression of senescence marker protein-30 (SMP30), as an anti-apoptotic marker, after irradiation to the liver. The livers of Smad3-mutant mice were exposed to local irradiation of 15 gray, from a 60Co-gamma radiation. One week after irradiation, in Smad3-KO mice, radiation-induced apoptosis was at lower levels compared to those of irradiated WT mice. These findings were well matched with the expression of CYP2E1, which plays a role in hepatic injuries produced by oxidative stress. In addition, antioxidant related protein, the SMP30 levels were reduced by gamma irradiation in both groups. Interestingly, the increased expression of SMP30 expression in Smad3-KO mice liver was preserved at a higher level than that of the WT mice after irradiation. Therefore, these results suggest that the interruption of TGF-β signaling by deletion of Smad3 brings about inhibition of hepatic apoptosis after ionizing irradiation. Moreover, the protective effect to ionizing radiation might be in correlation with the overexpression of SMP30 in the Smad3-null mice, which may act as an anti-apoptotic signaling molecule. The alteration of SMP30 by interruption of Smad3 might be a useful therapeutic target and diagnostic marker for radiation-induced liver damages.
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Short Communication
  • Tetsuo NAKAJIMA, Keiko TAKI, Bing WANG, Tetsuya ONO, Tsuneya MATSUMOTO ...
    2008 Volume 49 Issue 6 Pages 661-666
    Published: 2008
    Released on J-STAGE: November 28, 2008
    Advance online publication: October 29, 2008
    JOURNAL FREE ACCESS
    The health effects of low-dose radiation exposure are of public concern. Although molecular events in the cellular response to high-dose-rate radiation exposure have been fully investigated, effects of long-term exposure to extremely low-dose-rate radiation remain unclear. Protein expression was analyzed by two-dimensional electrophoresis in livers from mice irradiated for 485 days (22 hr/day) at low-dose-rates of 0.032 μGy/min, 0.65 μGy/min and 13 μGy/min (total doses of 21 mGy, 420 mGy and 8000 mGy, respectively). One of the proteins that showed marked changes in expression was identified as rhodanese (thiosulfate sulfurtransferase). Rhodanese expression was increased after irradiation at 0.65 μGy/min and 13 μGy/min, while its expression was not changed at 0.032 μGy/min. Rhodanese is a detoxification enzyme, probably related to the regulation of antioxidative function. However, antioxidative proteins, such as superoxide dismutase (SOD)1 (also known as Cu,Zn-SOD) and SOD2 (also known as Mn-SOD), which can be induced by high-dose-rate radiation, were not induced at any low-dose-rates tested. These findings indicate that rhodanese is a novel protein induced by low-dose-rate radiation, and further analysis could provide insight into the effects of extremely low-dose-rate radiation exposure.
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