• Title/Summary/Keyword: Radiation-induced adaptive response

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INVOLVEMENT OF p27CIP/KIP IN HSP25 OR INDUCIBLE HSP70 MEDIATED ADAPTIVE RESPONSE BY LOW DOSE RADIATION

  • Seo, Hang-Rhan;Chung, Hee-Yong;Lee, Yoon-Jin;Baek, Min;Bae, Sang-Woo;Lee, Su-Jae;Lee, Yun-Sil
    • Nuclear Engineering and Technology
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    • v.38 no.3
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    • pp.285-292
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    • 2006
  • Thermoresistant (TR) clones of radiation-induced fibrosarcoma (RIF) cells have been reported to show an adaptive response to 1cGy of low dose radiation, and HSP25 and inducible HSP70 are involved in this process. In this study, to further elucidate the mechanism by which HSP25 and inducible HSP70 regulate the adaptive response, HSP25 or inducible HSP70 overexpressed RIF cells were irradiated with 1cGy and the cell cycle was analyzed. HSP25 or inducible HSP70 overexpressed cells together with TR cells showed increased G1 phase after 1cGy irradiation, while RIF cells did not. $[^3H]-Thymidine$ and BrdU incorporation also indicated that both HSP25 and inducible HSP70 are involved in G1 arrest after 1cGy irradiation. Molecular analysis revealed upregulation of p27Cip/Kip protein in HSP25 and inducible HSP70 overexpressed cells, and cotransfection of p27Cip/Kip antisense abolished the induction of the adaptive response and 1cGy-mediated G1 arrest. The above results indicate that induction of an adaptive response by HSP25 and inducible HSP70 is mediated by upregulation of p27Cip/Kip protein, resulting in low dose radiation-induced G1 arrest.

Effects of Inhibitors on Cross-Adaptive Response to Ultraviolet Radiation or Ethyl methanesulfonate in Chinese Hamster Ovary Cells

  • Lee, Dong-Wook;Shin, Eun-Joo;Kim, Seon-Young;Um, Kyung-Il
    • Environmental Mutagens and Carcinogens
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    • v.16 no.2
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    • pp.83-87
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    • 1996
  • This study was performed by the sister chromatid exchanges (SCEs) to investigate the effects of Aphidicolin (APC) or 2, 4-dinitrophenoi (DNP) on cross-adaptive response to ultraviolet radiation (UV) or ethyl methanesulfonate (EMS) in Chinese hamster ovary (CHO) cells. The pretreatment with 1 J/m$^2$ UV decreased the yield of SCEs induced by subsequent treatment with 8 mM EMS in CHO cells. And the treatment with 10 $\mu$g/ml APC or 50 $\mu$M DNP during incubation after pretreatment with 1 J/m$^2$ UV increased the yield of SCEs induced by 8 mM EMS. The pretreatment with 2 mM EMS decreased the yield of SCEs induced by subsequent treatment with 5 J/m$^2$ UV. The treatment with 10 $\mu$g/ml APC during incubation after 2 mM EMS increased the yield of SCEs induced by 5 J/m$^2$ UV. These results suggest that APC and DNP inhibit cross-adaptive response to pretreatment with UV and subsequent treatment with EMS, and also cross-adaptive response to pretreatment with EMS and subsequent treatment with UV is inhibited by APC in CHO cells.

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Low-dose of Ultraviolet radiation-, Ethyl methanesulfonateor Bleomycin-lnduced Adaptive Response in Chinese hamster ovary Cells

  • Lee, Dong-Wook;Shin, Eun-Joo;Um, Kyung-Il
    • Environmental Mutagens and Carcinogens
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    • v.15 no.2
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    • pp.94-99
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    • 1995
  • The adaptive response and cross-adaptive response to sister chromatid exchanges (SCEs) and DNA single-strand breaks (SSBs) in Chinese hamster ovary (CHO)-K$_1$ cells treated with ultraviolet radiation (UV), ethyl methanesuffonate (EMS), or bleomycin (BLM) were investigated. Two assays were used in this study; SCEs and alkaline elution. The pretreatment with low conditioning dose of 2 mM EMS or 1 J/m$^2$ UV decreased the yield of SCEs induced by subsequent treatment with 8 mM EMS, 5 J/m$^2$ UV or 5 $\mu$g/ml BLM. And the pretreatment with low conditioning dose of 1 $\mu$g/ml BLM decreased the yield of SCEs induced by subsequent treatment with 5 $\mu$g/ml BLM or 5 J/m$^2$ UV. The rejoining of DNA SSBs in cells subsequently treated with 2 J/m$^2$ UV, 50 mM EMS or 400 $\mu$g/ml BLM is higher than that only treated with 2 J/m$^2$ UV, 50 mM EMS or 400 $\mu$g/ml BLM. These results suggest that there are the adaptive response and cross-adaptive response to SCEs, and is the adaptive response to the rejoining of DNA SSBs in CHO cells.

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Pretreatment of Low Dose Radiation Reduces Radiation-Induced Apoptosis in Mouse Lymphoma (EL4) cells

  • Kim, Jeong-Hee;Hyun, Soo-Jin;Yoon, Moon-Young;Jioon, Young-Hoon;Cho, Chul-Koo;Yoo, Seong-Yul
    • Archives of Pharmacal Research
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    • v.20 no.3
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    • pp.212-217
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    • 1997
  • Induction of an adaptive response to ionizing radiation in mouse lymphoma (EL4) cells was studied by using cell survival fraction and apoptotic nucleosomal DNA fragmentation as biological end points. Cells in early log phase were pre-exposed to low dose of ${\gamma}$-rays (0.01 Gy) 4 or 20 hrs prior to high dose ${\gamma}$-ray (4, 8 and 12 Gy for cell survival fraction analysis; 8 Gy for DNA fragmentation analysis) irradiation. Then cell survival fractions and the extent of DNA fragmentation were measured. Significant adaptive response, increase in cell survival fraction and decrease in the extent of DNA fragmentation were induced when low and high dose .gamma.-ray irradiation time interval was 4 hr. Addition of protein or RNA synthesis inhibitor, cycloheximide or 5,6-dichloro-1-.betha.-d-ribofuranosylbenzimidazole (DRFB), respectively during adaptation period, the period from low dose ${\gamma}$-ray irradiation to high dose ${\gamma}$-ray irradiation, was able to inhibit the induction of adaptive response, which is the reduction of the extent DNA fragmentation in irradiated EL4 cells. These data suggest that the induction of adaptive response to ionizing radiation in EL4 cells required both protein and RNA synthesis.

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Adaptive Response Induced by Low Dose Ionizing Radiation in Human Lymphocytes (인체 말초 혈액 림프구에서 저선량 방사선 조사에 의해 유도되는 적응 반응)

  • Kim, Jeong-Hee;Lee, Kyung-Jong;Cho, Chul-Koo;Yoo, Seong-Yul;Kim, Tae-Hwan;Kim, Sung-Ho
    • Journal of Radiation Protection and Research
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    • v.20 no.2
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    • pp.97-102
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    • 1995
  • Adaptive response induced by low dose ${\gamma}-ray$ irradiation in human peripheral lymphocytes was examimed. Human lymphocytes were exposured to low dose of ${\gamma}-ray$ (priming dose, 0.01Gy) followed by high dose (challenging dose, 1.5Gy) after various time intervals (4, 7, 20 hours). Frequencies of micronuclei were enumerated in both primed and unprimed groups. Maximum reduction in frequency of micronuclei was observed when challenging dose irradiation was followed by priming dose after 4hr incubation period. When challenging doses were irradiated 7 or 20hr after priming dose, frequencies of micronuclei were reduced slighty. However, these reduction were not statistically significant. In this study, human peripheral lymphocytes were irradiated at Go phase and they showed adaptive response induced by low dose radiation. Since micronucleus assay is relatively simpler and faster than other methods, it may be a good tool for evaluating radiation-induced adaptive responses.

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Effect of Small Dose of Radiation on Induction of Apoptosis in Murine Tumors (마우스 종양에서 저선량 방사선이 Apoptosis의 유도에 미치는 영향)

  • Seong, Jin-Sil;Pyo, Hong-Ryull;Chung, Eun-Ji;Kim, Sung-Hee;Suh, Chang-Ok
    • Radiation Oncology Journal
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    • v.17 no.4
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    • pp.307-313
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    • 1999
  • Purpose : To investigate the Presence of adaptive response by low dose radiation in murine tumors in relation to radiation induced apoptosis as well as related mechanism. Materials and Methods : Syngeneic murine tumors, OCa-I and HCa-l, were given 0.05 Gy pretreatment followed by therapeutic dose of 25 Gy radiation. Induction of apoptosis was analyzed for each treatment group. Regulating molecules of apoptosis, p53, Bcl-2, Bax, Bcl-X, were also analyzed by Western blotting. Results : In 0.05 Gy pretreatment group of OCa-I, 25 Gy-induced apoptosis per 1000 cells was 229, which was estimated at $30\%$ lower level than the expected (p<0.05). In contrast, this reduction in radiation induced apoptosis was not seen in HCa-l. In the expression of apoptosis regulating molecules, p53 increased in both tumors in response to radiation. Bcl-2 and Bax did not show significant change in both tumors however, the expression of Bcl-2 surpassed that of Bax in 0.05 Gy pretreatment group of OCa-l. Bcl-X was not expressed in OCa-l. In HCa-l, Bcl-X showed increased expression even with 0.05 Gy. Conclusion : Adaptive response by low dose radiation Is shown in one murine tumor, OCa-l, in relation to radiation induced apoptosis. Apoptosis regulating molecules including Bcl-2/Bax and Bcl-X, appear to related. This study shows an evidence that adaptive response is present, but not a generalized phenomenon in vivo.

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Adaptive Response Induced by Low Dose Ionizing Raditation in Human Cervical Carcinoma Cells

  • Kim, Jeong -Hee;Lee, Kyung -Jong;Cho, Chul -Koo;Yoo, Seong -Yul;Kim, Tae -Hwan;Ji, Young -Hoon;Kim, Sung -Ho
    • Archives of Pharmacal Research
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    • v.18 no.6
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    • pp.410-414
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    • 1995
  • Adaptive response induced by low dese .gamma.-ray irradiation in human cervical carcinoma cells was examined. Cells were exposured to low dose of .gamma.-ray irradiation in human cervical carcinoma cells was examined. Cells were exposured to low dose of .gamma.-ray (1-cGy) followed by high doses of r-ray irradiation (0,1,2,3,5,7 and 9Gy for chlnogenic assay or 1.5Gy for micronucleus assay) with various time intervals. Survival fractions of cells in both low dose-irradiated and unirrated groups were analyzed by clonogenic assay. Surviva fractions of low dose-irradiated in cell survival was maximum when low and high dose irradiation time interval was 4 hr. Frequencies of micronuclei which is an indicative of chromosome aberration were also enutained from survival fractions analyzed by clonogenic assay, maximum when low and high dose irradiation time interval was 4hr. Frequencies of micronuclei which is an indicative of chromosome aberration were also enumerated in both low dose-irradiated and unirradiated groups. In consiststent with the result obtained from survival fractions analyzed by clonogenic assay, maximum reduction in frquencies of micronuclei was observed when low dose radiation was given 4 hr prior to high response to subsequent high dose .gamma.-ray irradiation in human cervical carcinomal cells. Our data suggest that one of the possible mechanisms of adaptive response induced by low dose rediation is the increase in repair of DNA double strand breaks in low dose radiation-adapted cells.

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Adaptive Response to ionizing Radiation Induced by Low Doses of Gamma Rays in Human Lymphoblastoid Cell Lines (인체임파양세포에서 저선량의 감마선에 의해서 유도되는 적응 반응)

  • Seong, Jin-Sil;Suh, Chang-Ok;Kim, Gwi-Eon
    • Radiation Oncology Journal
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    • v.12 no.1
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    • pp.1-8
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    • 1994
  • When cells are exposed to low doses of a mutagenic or clastogenic agents. they often become less sensitive to the effects of a higher dose administered subsequently. Such adaptive responses were first described in Escherichia coli and mammalian cells to low doses of an alkylating agent. Since most of the studies have been carried out with human lymphocytes, it is urgently necessary to study this effect in different cellular systems. Its relation with inherent cellular radiosensitivity and underlying mechanism also remain to be answered. In this study, adaptive response by 1 cGy of gamma rays was investigated in three human lymphoblastoid cell lines which were derived from ataxia telangiectasia homozygote, ataxia telangiectasia heterozygote, and normal individual. Experiments were carried out by delivering 1 cGy followed by 50 cGy of gamma radiation and chromatid breaks were scored as an endpoint. The results indicate that prior exposure to 1 cGy of gamma rays reduces the number of chromatid breaks induced by subsequent higher dose (50 cGy), The expression of this adaptive response was similar among three cell lines despite of their different radiosensitivity. When 3-aminobenzamide, an inhibitor of poly (ADP-ribose) polymerase, was added after 50 cGy, adaptive responses were abolished in all the tested cell lines. Therefore it is suggested that the adaptive response can be observed in human lymphoblastoid cell lines, which was first documented through this study. The expression of adaptive response was similar among the cell lines regardless of their radiosensitivity. The elimination of the adaptive response by 3-aminobenzamide is consistent with the proposal that this adaptive response is the result of the induction of a certain chromosomal repair mechanism.

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Ultraviolet Radiation-Induced Apoptosis is Inversely Correlated with the Expression Level of Poly(ADP-ribose) Polymerase

  • Oh, Kyu Seon;Lee, Dong Wook;Chang, Jeong Hyun;Moon, Yong Suk;Um, Kyung ll
    • Animal cells and systems
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    • v.5 no.1
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    • pp.77-83
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    • 2001
  • The present study was conducted to elucidate whether the expression level of poly(ADP-ribose) polymerase (PARP) is related to the ultraviolet radiation (UV)-induced apoptosis. After treatment of the mammalian cell lines HeLa S3 and Chinese hamster ovary (CHO) with 50 J/m2 UV, induction of apoptosis was determined by several means during 24 h post-incubation. Incidence of apoptosis was much lower in CHO than HeLa S3 cells based on the percentage of apoptotic cells in terms of morphological changes in nucleus or direct counting of viable cells and qualitative or quantitative DNA fragmentation. Interestingly, when the expression level of PARP was measured by western blotting, the amounts of PARP that was retained at each time point inversely correlated with the incidences of apoptosis in these cells. Concomitant with generation of the 85 kDa fragment, 116 kDa PARP disappeared in HeLa S3 within 6 h after UV treatment, whereas a fair amounts of 116 kDa band was still retained in CHO cells at 36 h post-incubation. This inverse relationship was also observed in the adaptive response system, in which cells weve treated with a high dose of UV after pretreatment with a low dose. As expected, typical adaptive responses appeared in CHO cells but not in HeLa cells, showing greater cell viability and lesser DNA fragmentation. During the adaptive response in CHO cells, PARP was expressed at much higher level compared to the single, high dose-treated cells. Interestingly, even though PARP was induced at 6 h post-incubation In both cell types, its expression was more prominent in CHO cells. Thus, our data indicate that the retained level of intact PARP against UV damage inversely correlates with incidence of apoptosis in mammalian cells, and also suggest that a machinery to protect the PARP degradation against UV damage exists in CHO but not in HeLa S3 cells.

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