• Journal of Microbiology and Biotechnology
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• v.18 no.3
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• pp.523-531
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• 2008

Radiotherapy is currently applied in the treatment of human cancers. We studied whether genistein would enhance the radiosensitivity and explored its precise molecular mechanism in cervical cancer cells. After co-treatment with genistein and irradiation, the viability, cell cycle analysis, and apoptosis signaling cascades were elucidated in CaSki cells. The viability was decreased by co-treatment with genistein and irradiation compared with irradiation treatment alone. Treatment with only ${\gamma}$-irradiation led to cell cycle arrest at the $G_1$ phase. On the other hand, co-treatment with genistein and ${\gamma}$-irradiation caused a decrease in the $G_1$ phase and a concomitant increase up to 56% in the number of $G_2$ phase. In addition, co-treatment increased the expression of p53 and p21, and Cdc2-tyr-15-p, supporting the occurrence of $G_2/M$ arrest. In general, apoptosis signaling cascades were activated by the following events: release of cytochrome c, upregulation of Bax, down regulation of Bcl-2, and activation of caspase-3 and -8 in the treatment of genistein and irradiation. Apparently, co-treatment downregulated the transcripts of E6*I, E6*II, and E7. Genistein also stimulated irradiation-induced intracellular reactive oxygene, species (ROS) production, and co-treatment-induced apoptosis was inhibited by the antioxidant N-acetylcysteine, suggesting that apoptosis has occurred through the increase in ROS by genistein and ${\gamma}$-irradiation in cervical cancer cells. Gamma-irradiation increased cyclooxygenase-1 (COX-2) expression, whereas the combination with genistein and ${\gamma}$-irradiation almost completely prevented irradiation-induced COX-2 expression and $PGE_2$ production. Co-treatment with genistein and ${\gamma}$-irradiation inhibited proliferation through $G_2/M$ arrest and induced apoptosis via ROS modulation in the CaSki cancer cells.

• Journal of Korean Neurosurgical Society
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• v.37 no.1
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• pp.48-53
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• 2005

Objective: The purpose of this study is to elucidate in vitro responses to combined gamma knife irradiation and p53 gene transfection on human malignant glioma cell lines. Methods: Two malignant human glioma cell lines, U87MG (p53-wild type) and U373MG (p53-mutant) were transfected with an adenoviral vector containing p53 (MOI of 50) before and after applying 20Gy of gamma irradiation. Various assessments were performed, including, cell viability by MTT assay; apoptosis by annexin assay; and cell cycle by flow cytometry, for the seven groups: mock, p53 only, gamma knife (GK) only, GK after LacZ, LacZ after GK, GK after p53, p53 after GK. Results: Cell survival decreased especially, in the subgroup transfected with p53 after gamma irradiation. Apoptosis tended to increase in p53 transfected U373 MG after gamma irradiation (apoptotic rate, 38.9%). The G2-M phase cell cycle arrest markedly increased by transfecting with p53, 48 hours after gamma knife irradiation in U373 MG (G2-M phase, 90.8%). Conclusion: These results suggest that the in vitro effects of combined gamma knife irradiation and p53 gene transfection is an augmentation of apoptosis and G2-M phase cell cycle arrest, which are more exaggerated in U373 MG with p53 transfection after gamma knife irradiation.

• Biomolecules & Therapeutics
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• v.21 no.3
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• pp.210-215
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• 2013

Ionizing radiation can induce cellular oxidative stress through the generation of reactive oxygen species, resulting in cell damage and cell death. The aim of this study was to determine whether the antioxidant effects of the flavonoid fisetin (3,7,3',4'-tetrahydroxyflavone) included the radioprotection of cells exposed to ${\gamma}$-irradiation. Fisetin reduced the levels of intracellular reactive oxygen species generated by ${\gamma}$-irradiation and thereby protected cells against ${\gamma}$-irradiation-induced membrane lipid peroxidation, DNA damage, and protein carbonylation. In addition, fisetin maintained the viability of irradiated cells by partially inhibiting ${\gamma}$-irradiation-induced apoptosis and restoring mitochondrial membrane potential. These effects suggest that the cellular protective effects of fisetin against ${\gamma}$-irradiation are mainly due to its inhibition of reactive oxygen species generation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.5
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• pp.1256-1260
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• 2005

The purpose of this study was to investigate the effects of Angelica gigas on jejunal survival, endogenous spleen colony formation and jejunal crypt cells of mice irradiated with Gamma-ray irradiation. The subject of this study includes 42 mice which were divided into each 7 groups. Angelica gigas experiment groups were Angelica gigas + Gamma-ray(10Gy), Angelica gigas + Gamma-ray(3Gy), Angelica gigas. Gamma-ray(1 Gy), Gamma-ray control (10Gy), Gamma-ray control(3Gy), Gamma-ray control(1Gy), Normal groups. In the present study to evaluate the effect of Angelica gigas on jejunal crypt survival, endogenous spleen colony formation, and apoptosis in jejunal crypt cells of mice Gamma-ray with each dose of Gamma-ray irradiation. The results of this study were as follows: In low-dose(1Gy) Gamma-ray radiation were treatment of Angelica gigas showed significantly increased(p<0.05) on the cell death apoptosis in crypt, intestine crypts survival of intestine after gamma-ray irradiation. High-dose(10Gy) Gamma-ray, treatment of Angelica gigas showed significantly increased(p<0.05) on the leukocyte. The above results suggest that Angelica gigas were immunostimulating effectively reduced Gamma-ray irradiation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.3
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• pp.670-674
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• 2006

This experimental study was carried out to investigate the immunostimulating effect of Acanthopanax, as Oriental rhizomata herbs, on jejunal survival, endogenous spleen colony formation, apoptosis in jejunal crypt cells and lipid peroxidation in the liver of mice following Gamma-ray irradiation. The subject of this study includes 72 mice which were divided into each 7 groups. Acanthopanax experiment groups were Acanthopanax. Gamma-ray(lOGy), Acanthopanax. Gamma-ray(3Gy), Acanthopnax. Gamma-ray(1Gy), Gamma-ray control(1OGy), Gamma-ray control(3Gy), Gamma-ray control(1Gy), Normal groups. The results of this study were as follows : Treatment with Acanthopanax showed significantly increased(p<0.05) on the cell death apoptosis in crypt, intestine crypts survival of intestine in mice following low-dose(1Gy) Gamma-ray radiation. And that significantly increased(p<0.05) on jejunal crypt survival and reduced(p<0.05) on lipid peroxidation in mice following high-dose(1OGy) Gamma-ray radiation. The above results suggest that Acathopanax were immunostimulating effectively reduced Gamma-ray irradiation.

• Journal of Life Science
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• v.18 no.8
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• pp.1042-1048
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• 2008

Prostate cancer is the most predominant cancer in men and related death rate increases every year. Till date, there is no effective therapy for androgen independent prostate cancer. To investigate the mechanism for cell growth inhibition or apoptosis in human androgen independent prostate cancer PC-3 cells after gamma irradiation. The aim of this study was to examine the potential of gamma irradiation to induce apoptosis in PC-3 cells and to assess the mechanism of gamma irradiation-induced apoptosis. Five different assays were employed in this study: cell proliferation assay, morphological assessments of apoptotic cells, DNA fragmentation analysis, quantification of apoptosis by annexin V (AV) and propidium iodide (PI) staning, and western blot analysis. Cell viability was inversely related to radiation dose. DAPI-positive cells were detected 48 hr after 40 Gy radiation exposure. And nuclear morphological changes of cells were observed by gamma irradiation. DNA ladder patterns in the cells exposed to gamma-radiation were appeared at 24 hr. Also, gamma irradiation induces apoptosis of PC-3 cells via Caspase3, Bax and PARP-dependent fashion.

• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.633-639
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• 2003

We investigated the effect of green tea and its fractions of alcohol and polysaccharide on jejunal crypt survival, endogenous spleen colony formation, and apoptosis in jejunal crypt cells of mice irradiated with high and low dose of gamma-irradiation. Jejunal crypts were protected by pretreatment of green tea (i.p.: 50 mg/kg of body weight, at 12 and 36 hours before irradiation., p.o.: 1.25% water extract, for 7days before irradiation, p<0.01) and alcohol and polysaccharide fractions showed no significant modifying effects. Green tea and its fractions administration before irradiation (i.p. at 12 and 36hours before irradiation) resulted in an increase of the formation of endogenous spleen colony (p<0.05). The frequency of radiation-induced apoptosis in intestinal crypt cells was also reduced by pretreatment of green tea (i.p. at 12 and 36 hours before irradiation, p<0.05., p.o. for 7days before irradiation, p<0.001) and its fractions (p<0.001). These results indicated that green tea might be a useful radioprotector, especially since it is a relatively nontoxic natural product. Further studies are needed to characterize better the promotion nature of green tea and its components.

• Journal of Life Science
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• v.19 no.6
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• pp.799-803
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• 2009

The killing of male germ cells by radiation and other toxicants has recently been attributed to apoptosis, but a critical evaluation of the presence of the different features of apoptosis in each epithelial stage has not been performed. In this study, mouse testes exposed to radiation were examined by light microscopy and terminal transferase-mediated end labeling (TUNEL) with periodic acid-Schiff (PAS) stains to determine whether the cells were apoptotic according to several criteria. Apoptosis was easily recognized by the presence of peroxidase-stained, entirely apoptotic bodies. In the TUNEL-positive cells or bodies, the stained products correlated precisely with the typical morphologic characteristics of apoptosis as seen at the light microscopic level. The changes that occurred from 0 to 24 hours after exposing the mice to 2 Gy of gamma-rays (2 Gy/min) were examined. The numbers of apoptotic cells reached a peak at 12 hours after irradiation and then declined. The mice that received 0-8 Gy of gamma-rays were examined 8 hours after irradiation. Dose-response relationships were generated for each stage of the epithelial cycle by counting TUNEL-positive cells. The dose-response curves were linear- quadratic [y=(-0.014${\pm}$0.009)$D^{2}$+(0.31${\pm}$0.697)D+0.3575. Where y=the number of apoptotic cells per seminiferous tubule, and D=the irradiation dose in Gy, $r^{2}$=0.9] and there was a significant relationship between the frequency of apoptotic cells and the radiation dose. Although the maximum response was produced by 8 Gy, even 0.5 Gy induced marked changes. These changes were most pronounced in B spermatogonia of stage V and the spermatocyte at the mitotic cells of stage XII.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.6
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• pp.816-822
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• 2015

The objective of this study was to evaluate the anticancer effects of gamma-irradiated apigenin against various human cancer cells. Structural changes were analyzed by high pressure liquid chromatography. Gamma-irradiated apigenin showed a new peak distinguished from the main peak of apigenin (non-irradiated). Cytotoxic effects in human normal cells (HS68) were not observed upon gamma-irradiated and non-irradiated apigenin treatment. However, gamma-irradiated apigenin treatment significantly increased cytotoxicity against non-small lung cancer cells. For apoptosis induction activity tested by Annexin V/PI staining, gamma-irradiated apigenin showed a stronger effect than non-irradiated apigenin, and the level of reactive oxygen species was apparently elevated by gamma-irradiated apigenin treatment. These results suggest that gamma irradiation could be an effective method for development of a new physiological compound from an original compound by inducing structural changes.

• Korean Journal of Veterinary Research
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• v.39 no.3
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• pp.628-634
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• 1999

We have studied, by a nonisotopic in situ end-labeling(ISEL) technique, frequency of apoptosis in the external granular layer(EGL) of the cerebellum of immature mice by ${\gamma}$-rays irradiation from $^{60}Co$ or diagnostic ultrasound exposure. The total number of normal cells and cells showing morphological features of apoptosis were counted. The frequency of apoptotic cells was expressed as a percentage of the total number of cells in EGL. The extent of changes following 200 cGy(1090 cGy/min) was studied at 2, 4, 6, 8, 12, or 24 hours after exposure. The maximal frequency was found 6~8 hours after exposure. The immature mice that received 18, 36, 54, 108, 198, 396 cGy of ${\gamma}$-rays or diagnostic ultrasound(7.5MHz, 4.2mW, $I_{SPTA}=7.9mW/cm^2$, $I_{SPTA}=114.3W/cm^2$) for 10 or 30 minutes were examined 6 hours after irradiation. Measurements performed after ${\gamma}$-ray irradiation showed a dose-related increase in apoptotic cells in each of the mice studied. The dose-response curves were analyzed by a linear-quadratic model ; frequency of apoptotic cell in the EGL was y = $(0.1349{\pm}0.01175)D$+$(-0.0001522{\pm}0.0000334)D^2$+0.048($r^2$ = 0.981, D = dose in cGy). In the experiment of ultrasound exposure, the frequency of apoptotic cell was $0.106{\pm}0.130$(10 minutes exposure) and $0.167{\pm}0.220$(30 minutes exposure). We estimated the relative dose of the yield from the experiment with ultrasound by substituting the yield from ultrasound exposure into the curve from the ${\gamma}$-irradiation. The relative dose of ultrasound exposure compared with ${\gamma}$-irradiation were 0.432 cGy(10 minutes exposure) and 0.885 cGy(30 minutes exposure). We have found that there is no evidence to indicate that diagnostic ultrasound involves a significant risk.