• BMB Reports
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• v.47 no.10
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• pp.575-580
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• 2014

In this study, we investigate whether arsenite-induced DNA damage leads to p53-dependent premature senescence using human glioblastoma cells with p53-wild type (U87MG-neo) and p53 deficient (U87MG-E6). A dose dependent relationship between arsenite and reduced cell growth is demonstrated, as well as induced ${\gamma}H2AX$ foci formation in both U87MG-neo and U87MG-E6 cells at low concentrations of arsenite. Senescence was induced by arsenite with senescence-associated ${\beta}$-galactosidase staining. Dimethyl- and trimethyl-lysine 9 of histone H3 (H3DMK9 and H3TMK9) foci formation was accompanied by p21 accumulation only in U87MG-neo but not in U87MG-E6 cells. This suggests that arsenite induces premature senescence as a result of DNA damage with heterochromatin forming through a p53/p21 dependent pathway. p21 and p53 siRNA consistently decreased H3TMK9 foci formation in U87M G-neo but not in U87MG-E6 cells after arsenite treatment. Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage.

• Journal of Photoscience
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• v.9 no.2
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• pp.445-447
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• 2002

The compositional changes in mycosporine-like amino acids (MAAs) were investigated in the marine dinoflagellate Scrippsiella sweeneyae exposed to four different spectral compositions and five relative intensities of UV-B (280-320 nm) to UV-A (320-400 nm) + photosynthetically available radiation (PAR: 400-700 nm). Neither dose nor wavelengths of UVR significantly affected the growth rates. UVR caused a significantly increase in cell volume. Cell volume in the >280nm treatment was more than two times greater at 6.8 % of UVR intensity. Production of UVR induced MAAs was dependent on the dose of UVR. However. the induction of MAAs was related to the cell growth. Greater induction of MAAs was observed at shorter wavelengths. The composition of MAAs varied with increasing light intensity of UVR.

• Radiation Oncology Journal
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• v.7 no.1
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• pp.1-13
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• 1989

Effects of ionizing radiation alone and combined with chemotherapy on tumor growth and it's clonal specificity monitored by changes in distribution of chromosome number were studies in A549 ceil line originated from human adenocarcinoma of the lung. Radiation (300 rad, 600 rad and 900 rad) were delivered with or without 5-FU. Forty eight hours later, 57.5% of growth inhibition of cell w8s seen in cells treated with 5-FU concentration of $0.4{\mu}g/ml$ for 24hr exposure. Cell survival curves after radiation with and without 5-FU were made. Chromosomal analysis of cells in metaphase in control, and in cells treated with 300 rad of radiation, or $0.4{\mu}g/ml$ of 5-FU treatment, and combined treatment of both were done to examine the changes in ploidy and number of chromosome. Radiation combined with S-FU enhanced growth inhibition of A549 cells. However, no evidence of synergegic effects in growth. inhibition was observed in the cells treated with the combination therapy. Pattern of chromosomal distribution of survived cells were shifted from hyperploidy to hypoploidy by single dose of radiation (300 rad). As radiation dose increased a large number of hypoploidy cells were observed. Following treatment of cells with 5-FU, chomosomal distribution of survived cells were also shifted to hypodiploidy which were seen in cells treated with radiation, The ceil treated with 5-FU and fellowed by radiation within 24 hrs had cell with increased number of hypodiploidy cells. Almost same type of chromosomal changes were reproduced in cells treated with combined treatment with radiation and 5-FU. Minor differences were that cells with fewer number of chromosome were more frequent in cells treated with combined therapy. Further increase in cells of hypoploidy (93%) having 1-10 chromosome were induced by additional radiation. Therefore, the enhanced therapeutic effect of 5-FU combined with radiation of A549 cells appeared to be additive rather than synergistic.

• Korean Journal of Environmental Biology
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• v.22 no.4
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• pp.537-542
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• 2004

To reveal the relationship between the changes in the growth and photo- synthesis induced by low dose radiation, red pepper (Capsicum annuum L.) plants were serially irradiated three times with gamma rays of 0.5, 1, 2, 3, and 4 Gy. The plant growth was monitored by the fresh weight, the stem length, and the leaf length & width. All the irradiation groups (0.5-4 Gy) were stimulated in growth at 1 day after the $1^{st}$ irradiation (DA1I), but rather inhibited at 3 days after the $3^{rd}$ irradiation (DA3I). The maximum photochemical efficiency (Fv/Fm), the photochemical quenching (qP), the non-:photochemical quenching (NPQ) and the apparent rate of the photosynthetic electron transport (ETR) were used to represent the changes in the photosynthesis by the serial irradiation. The irradiation groups except 0.5 Gy had higher Fv/Fm values at 3 DA3I than the control one. After the 3$^{rd}$ irradiation, the qP values appeared to be a little lower in the 1-4 Gy groups than in the control and 0.5 Gy ones. In contrast, the NPQ values were rather higher in the irradiation groups except 0.5 Gy. During the whole experimental period, the ETRs decreased in the control group but remained relatively constant in the 4-Gy one. In conclusion, the results obtained indicate that the stimulatory effect of ionizing radiation on the plant growth was determined by the incident dose of the single irradiation rather than by the cumulative one of the serial irradiation. They also demonstrate that the growth stimulation induced by a low dose radiation could not be positively correlated with an alteration in the photosynthesis. Additionally, we discuss in text that an ionizing radiation may partly protect the leaf senescence by delaying the development of the plants.

• Radiation Oncology Journal
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• v.32 no.4
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• pp.262-265
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• 2014

Tamoxifen and radiotherapy are used in breast cancer treatment worldwide. Radiation recall dermatitis (RRD), induced by tamoxifen, has been rarely reported. Herein, we report a RRD case induced by tamoxifen. A 47-year-old woman had a right quadrantectomy and an axillary lymph node dissection due to breast cancer. The tumor was staged pT2N0; it was hormone receptor positive, and human epidermal growth factor receptor 2 negative. The patient received adjuvant chemotherapy followed by tamoxifen and radiotherapy. After 22 months of tamoxifen, the patient developed a localized heating sensation, tenderness, edema, and redness at the irradiated area of the right breast. The symptoms improved within 1 week without treatment. Three weeks later, however, the patient developed similar symptoms in the same area of the breast. She continued tamoxifen before and during dermatitis, and symptoms resolved within 1 week.

• Radiation Oncology Journal
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• v.33 no.4
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• pp.328-336
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• 2015

Purpose: Past studies have reported that S-allylcysteine (SAC) inhibits the migration and invasion of cancer cells through the restoration of E-cadherin, the reduction of matrix metalloproteinase (MMP) and Slug protein expression, and inhibition of the production of reactive oxygen species (ROS). Furthermore, evidence is emerging that shows that ROS induced by radiation could increase Met activation. Following on these reports of SAC and Met, we investigated whether SAC could suppress Met activation. Materials and Methods: Wound healing, invasion, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium (MTT), soft agar colony forming, western blotting, and gelatin zymography assays were performed in the human nasopharyngeal cancer cell lines HNE1 and HONE1 treated with SAC (0, 10, 20, or 40 mM) and hepatocyte growth factor (HGF). Results: This study showed that SAC could suppress the migration and invasion of HNE1 and HONE1 cell lines by inhibiting p-Met. An increase of migration and invasion induced by HGF and its decrease in a dose dependent manner by SAC in wound healing and invasion assays was observed. The reduction of p-Met by SAC was positively correlated with p-focal adhesion kinase (p-FAK) and p-extracellular related kinase (p-ERK in both cell lines). SAC reduced Slug, MMP2, and MMP9 involved in migration and invasion with the inhibition of Met-FAK signaling. Conclusion: These results suggest that SAC inhibited not only Met activation but also the downstream FAK, Slug, and MMP expression. Finally, SAC may be a potent anticancer compound for nasopharyngeal cancer treated with radiotherapy.

• Radiation Oncology Journal
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• v.20 no.3
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• pp.253-263
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• 2002

Purpose : In order to understand in vivo radiation damage modifying of bFGF on jejunal mucosa, bone marrow and the effect of bFGF on the growth of transplanted mouse sarcoma 180 tumor in mice. Materials and Methods : Mice were treated with $6\;{\mu}g$ of bFGF at 24 hours and 4 hours before exposing to 600 cGy, 800 cGy and 1,000 cGy total body irradiation (TBI), and then exposed to 3,000 cGy local radiation therapy on the tumor bearing thigh. Survival and tumor growth curve were plotted in radiation alone group and combined group of bFGF and irradiation (RT). Histologic examination was performed in another experimental group. Experimental groups consisted of normal control, tumor control, RT (radiation therapy) alone, $6\;{\mu}g$ bFGF alone, combined group of $3\;{\mu}g$ bFGF and irradiation (RT), combined group of $6\;{\mu}g$ bFGF and irradiation (RT). Histologic examination was peformed with H-E staining in marrow, jejunal mucosa, lung and sarcoma 180 bearing tumor. Radiation induced apoptosis was determined in each group with the DNA terminal transferase nick-end labeling method ($ApopTag^{\circledR}$ S7100-kit, Intergen Co.) Results : The results were as follows 1) $6\;{\mu}g$ bFGF given before TBI significantly improved the survival of lethally irradiated mice. bFGF would protect against lethal bone marrow syndrome. 2) $6\;{\mu}g$ bFGF treated group showed a significant higher crypt depth and microvilli length than RT alone group (p<0.05). 3) The bone marrow of bFGF treated group showed less hypocellularity than radiation alone group on day 7 and 14 after TBI (p<0.05), and this protective effect was more evident in $6\;{\mu}g$ bFGF treated group than that of $3\;{\mu}g$ bFGF treated group. 4) bFGF protected against early radiation induced apoptosis in intestinal crypt cell but might have had no antiapoptotic effect in bone marrow stem cell and pulmonary endothelial cells. 5) There was no significant differences in tumor growth rate between tumor control and bFGF alone groups (p>0.05). 6) There were no significant differences in histopathologic findings of lung and mouse sarcoma 180 tumor between radiation alone group and bFGF treated group. Conclusions : Our results suggest that bFGF protects small bowel and bone marrow from acute radiation damage without promoting the inoculated tumor growth in C3H mice. Improved recovery of early responding normal tissue and reduced number of radiation induced apoptosis may be possible mechanism of radioprotective effect of bFGF.

• Korean Journal of Environmental Agriculture
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• v.19 no.5
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• pp.394-400
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• 2000

${\gamma}-Radiation$ at very low doses frequently has a stimulating or hormetic effect on the growth of organism. Effects of low dose ${\gamma}-ray$ irradiation on the root growth of soybean cultivars were investigated and hormetic effects by environmental conditions were compared with the occurrence of increased economic yield, seeds of cultivars were irradiated with the dose of $0.5{\sim}20Gy$ and cultivated in growth chamber controling temperature, humidity, light, greenhouse and field respectively. To understand hormetic effect on root growth of cultivars and the difference of hormetic effect by cultivation environment, harvested root of soybean cultivars were scanned with image file, and root surface area, root length, root average diameter etc. were examined by WinRhizo program. Also, dry weight of cultivars was examined. Root growth and dry weight of soybean cultivars showed apparently hormetic effect at cultivation of growth chamber condition. In field experiment executed for whole life cycle, yields of pea were not different significantly in each ${\gamma}-ray$ irradiated cultivars but weight of one hundred peas increased in whole ${\gamma}-ray$ irradiated cultivars. Increment of yield was assumed to be induced through shortening of maturing stage caused by ${\gamma}-ray$ hormesis in early growth stage.

• Archives of Plastic Surgery
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• v.45 no.5
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• pp.403-410
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• 2018

Background Radiation-induced skin injury is a dose-limiting complication of radiotherapy. To investigate this problem and to develop a framework for making decisions on treatment and dose prescription, a murine model of radiation-induced skin injury was developed. Methods The dorsal skin of the mice was isolated, and irradiation was applied at single doses of 15, 30, and 50 Gy. The mice were followed for 12 weeks with serial photography and laser Doppler analysis. Sequential skin biopsy samples were obtained and subjected to a histological analysis, immunostaining against transforming growth factor beta (TGF-${\beta}$), and Western blotting with Wnt-3 and ${\beta}$-catenin. Increases in the levels of TGF-${\beta}$, Wnt, and ${\beta}$-catenin were detected after irradiation. Results All tested radiation doses caused progressive dermal thickening and fibrosis. The cause of this process, however, may not be radiation alone, as the natural course of wound healing may elicit a similar response. The latent appearance of molecular and histological markers that induce fibrosis in the 15 Gy group without causing apparent gross skin injuries indicates that 15 Gy is an appropriate dose for characterizing the effects of chronic irradiation alone. Thus, this model best mimics the patterns of injury that occur in human subjects. Conclusions This animal model can be used to elucidate the gross and molecular changes that occur in radiation-induced skin injury and provides an effective platform for studying this adverse effect without complicating the process of wound healing.

• Journal of Environmental Science International
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• v.21 no.12
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• pp.1435-1447
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• 2012

The present study was conducted to determine the effect of hexaconazole (HEX), a triazole fungicide, on the growth, yield, photosynthetic response and antioxidant potential in cucumber (Cucumis sativus L.) plants subjected to UV-B stress. UV-B radiation and HEX were applied separately or in combination to cucumber seedlings. The growth parameters were significantly reduced under UV-B treatment, however, this growth inhibition was less in HEX treated plants. HEX caused noticeable changes in plant morphology such as reduced shoot length and leaf area, and increased leaf thickness. HEX was quite persistent in inhibiting shoot growth by causing a reduction in shoot fresh and dry weight. HEX noticeably recovered the UV-B induced inhibition of biomass production. Significant accumutation in anthocyanin and flavonoid pigments in the leaves occurred as a result of HEX or UV-B treatments. HEX permitted the survival of more green leaf tissue preventing chlorophyll content reduction and higher quantum yield for photosystemII under UV-B exposure. HEX treatment induced a transient rise in ABA levels in the leaves, and combined application of HEX and UV-B showed a significant enhancement of ABA content which activates $H_2O_2$ generation. UV-B exposure induced accumulation of $H_2O_2$ in the leaves, while HEX prevented UV-B induced increase in $H_2O_2$, indicating that HEX serves as an antioxidant agent able to scavenge $H_2O$ to protect cells from oxidative damage. An increase in the ascorbic acid was observed in the HEX treated cucumber leaves affecting many enzyme activities by removing $H_2O_2$ during photosynthetic processes. The activities of antioxidant enzymes including catalase(CAT), ascorbate peroxidase(APX), superoxide dismutase(SOD) and peroxidase(POD) in the leaves in the presence of HEX under UV-B stress were higher than those under UV-B stress alone. These findings suggest that HEX may participate in the enhanced tolerance to oxidative stress. From these results it can be concluded that HEX moderately ameliolate the effect of UV-B stress in cucumber by improving the components of antioxidant defense system.