• The Korean Journal of Nuclear Medicine
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• v.26 no.1
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• pp.8-13
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• 1992

Low doses of ionizing radiation from external or internal sources cause heterogeneous distribution of energy deposition events in the exposed biological system. With the cell being the individual element of the tissue system, the fraction of cells hit, the dose received by the hit, and the biological response of the cell to the dose received eventually determine the effect in tissue. The hit cell may experience detriment, such as change in its DNA leading to a malignant transformation, or it may derive benefit in terms of an adaptive response such as a temporary improvement of DNA repair or temporary prevention of effects from intracellular radicals through enhanced radical detoxification. These responses are protective also to toxic substances that are generated during normal metabolism. Within a multicellular system, the probability of detriment must be weighed against the probability of benefit through adaptive responses with protection against various toxic agents including those produced by normal metabolism. Because irradiation can principally induce both, detriment and adaptive responses, one type of affected cells may not be simply summed up at the expense of cells with other types of effects, in assessing risk to tissue. An inventory of various types of effects in the blood forming system of mammals, even with large ranges of uncertainty, uncovers the possibility of benefit to the system from exposure to low doses of low LET radiation. This experimental approach may complement epidemiological data on individuals exposed to low doses of ionizing radiation and may lead to a more rational appraisal of risk.

• Proceedings of the Korean Radioactive Waste Society Conference
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• 2004.11a
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• pp.210.1-210.1
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• 2004

• Proceedings of the Korean Nuclear Society Conference
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• 2005.05a
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• pp.966-967
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• 2005

• Proceedings of the Korean Nuclear Society Conference
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• 2004.10a
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• pp.1135-1135
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• 2004

• 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.

• The Korean Journal of Nuclear Medicine
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• v.33 no.2
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• pp.172-177
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• 1999

Purpose: The purpose of this study was to ascertain whether radiation adaptive response could be induced by Tc-99m-methylene diphosphonate (Tc-99m-MDP) in peripheral lymphocytes of patients undergoing bone scintigraphy. Materials and Methods: Lymphocytes from 22 patients (6 males, 16 females, mean age $50{\pm}14$ years) were collected before and after bone scintigraphy using 740 MBq Tc-99m-MDP Lymphocytes from 10 controls (6 males, 4 females, mean age $43{\pm}7$ years) were also collected. They were exposed to challenge dose of 2 Gy gamma rays using a cell irradiator. Number of ring-form and dicentric chromosomes per 600 cells (chromosomal aberrations) was counted under the light microscope. Results: Chromosomal aberrations in patients before bone scintigraphy ($385.1{\pm}30.5$) was not different from that of controls ($367.8{\pm}36.6$). However, chromosomal aberrations in patients after bone scintigraphy was significantly decreased to $192.6{\pm}22.1$ (p=0.0001). Conclusion: Low dose gamma-irradiation by Tc-99m-MDP used for bone scintigraphy induces a cytogenetic adaptive response in peripheral lymphocytes.

• 대한핵의학회:학술대회논문집
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• 2000.05a
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• pp.71.2-71.2
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• 2000

• Journal of Radiation Protection and Research
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• v.28 no.2
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• pp.117-125
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• 2003

It was reported that radiopharamaceuticals induced radiation adaptive response (RAR) in patients undergoing nuclear medicine imaging studies. Individual variations of RAR were not studied well. The purpose of this study was to evaluate individual variation of RAR in patients undergoing nuclear medicine imaging studies. Peripheral lymphocytes were collected from 23 patients undergoing $^{99m}Tc-diethylenetriamine$ pentaacetic acid $(^{99m}Tc-DTPA)$ renal scintigraphy, 18 patients undergoing $^{99m}Tc-methylene$ diphosphonate $(^{99m}Tc-MDP)$ bone scintigraphy and 21 patients undergoing $^{99m}Tc-tetrofosmin\;(^{99m}Tc-TF)$ scintigraphy were collected before and 4 hours after injection of radiopharmaceuticals. The lymphocytes were exposed to challenge dose of 2 Gy gamma rays using a cell irradiator. Numbers of ring-form (R) and dicentric (D) chromosomes were counted under the light microscope. and used to calculate the frequency of chromosomal aberration [Ydr=(D+R)/total number of counted lymphocytes]. Adaptation index (k) was defined 3s ratio of Ydr in conditioned lymphocytes over Ydr in unconditioned lymphocytes. Coefficients of variance of k in $^{99m}Tc-DTPA,\;^{99m}Tc-MDP\;and\;^{99m}Tc-TF$ were 35%, 34% and 21%, respectively k was not dependent upon age, sex, and underlying diseases. There was a wide variation of RAR induced by radiopharmaceuticals among patients undergoing nuclear medicine procedures. It remains to be determined for causes of such variation.

• Korean Journal of Environmental Biology
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• v.22 no.3
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• pp.472-477
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• 2004

To study the radiation related gene expression in mutants of Bacillus lentimorbus WJ5 induced by gamm radiation, the simultaneous gene expression was analyzed by DNA micro array. We constructed DNA chips including two thousand randomly digested genome spots of B. lentimorbus WJ5 and compared its quantitative aspect with seven mutants induced by gamma radiation $(^{60}/Co)$. From the cluster analysis of gene expression pattern, totally 408 genes were expressed and 27 genes were significantly upregulated by the gamma radiation in all mutants. Especially, genes involved in repair (mutL, mutM), energy metabolism (acsA, sdhB, pgk, yhjB, citB), protease (npr), and reduction response to oxidative stress (HMM) were simultaneously upregulated. It seems that the induction of the direct and/or indirect repair related genes in mutants induced by gamma radiation could be remarkably different from the adaptive responses against acute exposure to radiation.

• Animal cells and systems
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• v.4 no.3
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• pp.293-297
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• 2000

The present investigation was performed to elucidate the effect of pretreatment with low dose ultraviolet radiation (UV) and ethyl methanesulfonate (EMS) on cell survival by trypan blue dye exclusion method and plasma membrane glycoconjugates by lectin-cytochemistry in sarcoma 180 (S180) cells. Pretreatment with 2 J/$m^2$ UV or 2 mM EMS increased the percentage of survival of cells subsequently treated with high dose UV (10 or 20 J/$m^2$) or EMS (10 or 20 mM), respectively. Staining intensity of concanavalin A (Con A) of the cells pretreated with 2J/$m^2$ UV or 2 mM EMS and subsequently treated with 10 or 20 mM EMS was stronger than that of the cellstreated with 10 or 20 mM EMS. These results suggest that there is an adaptive response on cell survival to EMS or UV in S180 cells. And the results show a change in mannose-containing glycoconjugates of plasma membrane in S180 cells pretreated with EMS or UV and subsequently treated with EMS.