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1.
Braz. j. med. biol. res ; 39(2): 227-236, Feb. 2006. tab, graf
Artigo em Inglês | LILACS | ID: lil-420274

RESUMO

Gamma-irradiation (gamma-IR) is extensively used in the treatment of hormone-resistant prostate carcinoma. The objective of the present study was to investigate the effects of 60Co gamma-IR on the growth, cell cycle arrest and cell death of the human prostate cancer cell line DU 145. The viability of DU 145 cells was measured by the Trypan blue exclusion assay and the 3(4,5-dimethylthiazol-2-yl)-2,5,diphenyltetrazolium bromide test. Bromodeoxyuridine incorporation was used for the determination of cell proliferation. Cell cycle arrest and cell death were analyzed by flow cytometry. Superoxide dismutase (SOD), specifically CuZnSOD and MnSOD protein expression, after 10 Gy gamma-IR, was determined by Western immunoblotting analysis. gamma-IR treatment had a significant (P < 0.001) antiproliferative and cytotoxic effect on DU 145 cells. Both effects were time and dose dependent. Also, the dose of gamma-IR which inhibited DNA synthesis and cell proliferation by 50 percent was 9.7 Gy. Furthermore, gamma-IR induced cell cycle arrest in the G2/M phase and the percentage of cells in the G2/M phase was increased from 15 percent (control) to 49 percent (IR cells), with a nonsignificant induction of apoptosis. Treatment with 10 Gy gamma-IR for 24, 48, and 72 h stimulated CuZnSOD and MnSOD protein expression in a time-dependent manner, approximately by 3- to 3.5-fold. These data suggest that CuZnSOD and MnSOD enzymes may play an important role in the gamma-IR-induced changes in DU 145 cell growth, cell cycle arrest and cell death.


Assuntos
Humanos , Masculino , Apoptose/efeitos da radiação , Ciclo Celular/efeitos da radiação , Proliferação de Células/efeitos da radiação , Raios gama , Neoplasias da Próstata/patologia , Superóxido Dismutase/efeitos da radiação , Western Blotting , Linhagem Celular Tumoral/efeitos da radiação , Neoplasias da Próstata/metabolismo
2.
Yonsei Medical Journal ; : 852-861, 2006.
Artigo em Inglês | WPRIM | ID: wpr-141741

RESUMO

This study investigated that whether a 2 mT, 60 Hz, sinusoidal electromagnetic field (EMF) alters the structure and function of cells. This research compared the effects of EMF on four kinds of cell lines: hFOB 1.19 (fetal osteoblast), T/G HA-VSMC (aortic vascular smooth muscle cell), RPMI 7666 (B lymphoblast), and HCN-2 (cortical neuronal cell). Over 14 days, cells were exposed to EMF for 1, 3, or 6 hours per day (hrs/d). The results pointed to a cell type-specific reaction to EMF exposure. In addition, the cellular responses were dependent on duration of EMF exposure. In the present study, cell proliferation was the trait most sensitive to EMF. EMF treatment promoted growth of hFOB 1.19 and HCN-2 compared with control cells at 7 and 14 days of incubation. When the exposure time was 3 hrs/d, EMF enhanced the proliferation of RPMI 7666 but inhibited that of T/G HA- VSMC. On the other hand, the effects of EMF on cell cycle distribution, cell differentiation, and actin distribution were unclear. Furthermore, we hardly found any correlation between EMF exposure and gap junctional intercellular communication in hFOB 1.19. This study revealed that EMF might serve as a potential tool for manipulating cell proliferation.


Assuntos
Humanos , Transdução de Sinais , Citoesqueleto de Actina/efeitos da radiação , Junções Comunicantes/metabolismo , Campos Eletromagnéticos , Proliferação de Células/efeitos da radiação , Fenômenos Fisiológicos Celulares/efeitos da radiação , Linhagem Celular , Diferenciação Celular/efeitos da radiação , Ciclo Celular/efeitos da radiação
3.
Yonsei Medical Journal ; : 852-861, 2006.
Artigo em Inglês | WPRIM | ID: wpr-141740

RESUMO

This study investigated that whether a 2 mT, 60 Hz, sinusoidal electromagnetic field (EMF) alters the structure and function of cells. This research compared the effects of EMF on four kinds of cell lines: hFOB 1.19 (fetal osteoblast), T/G HA-VSMC (aortic vascular smooth muscle cell), RPMI 7666 (B lymphoblast), and HCN-2 (cortical neuronal cell). Over 14 days, cells were exposed to EMF for 1, 3, or 6 hours per day (hrs/d). The results pointed to a cell type-specific reaction to EMF exposure. In addition, the cellular responses were dependent on duration of EMF exposure. In the present study, cell proliferation was the trait most sensitive to EMF. EMF treatment promoted growth of hFOB 1.19 and HCN-2 compared with control cells at 7 and 14 days of incubation. When the exposure time was 3 hrs/d, EMF enhanced the proliferation of RPMI 7666 but inhibited that of T/G HA- VSMC. On the other hand, the effects of EMF on cell cycle distribution, cell differentiation, and actin distribution were unclear. Furthermore, we hardly found any correlation between EMF exposure and gap junctional intercellular communication in hFOB 1.19. This study revealed that EMF might serve as a potential tool for manipulating cell proliferation.


Assuntos
Humanos , Transdução de Sinais , Citoesqueleto de Actina/efeitos da radiação , Junções Comunicantes/metabolismo , Campos Eletromagnéticos , Proliferação de Células/efeitos da radiação , Fenômenos Fisiológicos Celulares/efeitos da radiação , Linhagem Celular , Diferenciação Celular/efeitos da radiação , Ciclo Celular/efeitos da radiação
4.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 513-5, 2005.
Artigo em Inglês | WPRIM | ID: wpr-634815

RESUMO

The HL-60 cells were transfected with chk1 antisense and sense chain, and 24 h later subjected to irradiation. Twenty-four h after irradiation, the changes in the chk1 protein expression was assayed by Western blot, and the cell cycles and apoptosis rate detected by FCM. The irradiated apoptosis sensitivity was increased by antisense blocking of chk1 gene in HL-60 cell line with the apoptosis rate being 26.31%, significantly higher than that by the sense blocking (10.34%, 0.025 < P < 0.05). In HL-60 cells transfected with chk1 antisense chain, the G2/M phase arrest was attenuated and the cells in G2/M phase were accounted for 38.42%, significantly lower than those of the cells transfected with chkl sense chain (54.64%, 0.005 < P < 0.01). It was concluded that antisense blocking of chk1 gene could increase the apoptosis sensitivity to irradiation.


Assuntos
Apoptose/efeitos da radiação , Ciclo Celular/efeitos da radiação , Células HL-60 , Oligonucleotídeos Antissenso/genética , Proteínas Quinases/genética , Proteínas Quinases/metabolismo , Tolerância a Radiação/genética , Transfecção
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