Apoptosis ; radiation effects ; Cell Cycle ; radiation effects ; Cells, Cultured ; Electromagnetic Fields ; Gene Expression ; radiation effects ; Mutation ; radiation effects ; Recombination, Genetic ; radiation effects ; Yeasts ; cytology ; genetics ; radiation effects

Apoptosis ; radiation effects ; Calcium ; metabolism ; Cell Cycle ; radiation effects ; Cells, Cultured ; Electromagnetic Radiation ; Humans ; Lymphocytes ; metabolism ; pathology ; radiation effects

OBJECTIVETo explore the method of inducing and building pancreatic cancer cell sublines with radiation resistance.

METHODSSimulating the clinical radiotherapy, the pancreatic cell lines SW1990, Capan-1 (Cap), AsPC-1 (ASPC), P3, PANC-1 (Pan-1) and MIAPaCa-2 (MIA) were repeatedly given individual dose of X-rays with liner accelerator to induce radiation resistance, the changes of cell morphology, cell cycle and radio sensibility in the induced cell lines were compared with the parental cell lines at the end of inducing course.

RESULTSCompared with the parental cells, there were significant changes in morphology in the pancreatic cancer cell sublines after the radiation. Cell cycle analysis suggested that SW1990-R, ASPC-R, MIA-R, PAN-R and P3-R had lower G(2)/M and greater SF(2) (survival fraction after 2 Gy irradiation) compared with the parental cell lines.

CONCLUSIONSThe method of radiating cells step by step and repeatedly is viable to establish radio-resistant pancreatic cancer cell lines.

Cell Culture Techniques ; methods ; Cell Cycle ; radiation effects ; Cell Line, Tumor ; Cell Proliferation ; radiation effects ; Cell Shape ; radiation effects ; Cell Size ; radiation effects ; Cell Survival ; radiation effects ; Dose-Response Relationship, Radiation ; Humans ; Pancreatic Neoplasms ; pathology ; physiopathology ; Radiation Tolerance

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.
Signal Transduction ; Microfilaments/radiation effects ; Humans ; Gap Junctions/metabolism/radiation effects ; *Electromagnetic Fields ; Cell Proliferation/radiation effects ; Cell Physiology/*radiation effects ; Cell Line ; Cell Differentiation/radiation effects ; Cell Cycle/radiation effects

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.
Signal Transduction ; Microfilaments/radiation effects ; Humans ; Gap Junctions/metabolism/radiation effects ; *Electromagnetic Fields ; Cell Proliferation/radiation effects ; Cell Physiology/*radiation effects ; Cell Line ; Cell Differentiation/radiation effects ; Cell Cycle/radiation effects

OBJECTIVETo study the effects of extremely low frequency electromagnetic fields (ELF EMFs) on apoptosis and cell cycle of mouse brain and liver cells.

METHODSMice were exposed to 50 Hz, 0.2 mT or 6.0 mT electromagnetic fields for 2 weeks. TUNEL and flow cytometric methods were used to analyze apoptosis and cell cycle of brain and liver cells.

RESULTSAfter exposure to 0.2 mT and 6.0 mT ELF EMFs for 2 weeks, apoptosis rates of brain cells [(5.60 +/- 1.47)% and (4.73 +/- 0.48)% respectively] were higher than that of control [(2.90 +/- 0.75)%], and apoptosis rates of liver cells [(4.19 +/- 2.08)% and (3.38 +/- 0.65)% respectively] were higher than that of control [(1.84 +/- 0.76)%]. G0/G1 cell percentage of brain cells [(80.21 +/- 1.68)% and (79.54 +/- 0.56)% respectively] were higher than that of control [(76.85 +/- 0.83)%], and those of liver cells [(79.42 +/- 1.80)% and (80.47 +/- 1.79)% respectively] were higher than that of control [(73.36 +/- 3.10)%]. The above differences were all statistically significant as P < 0.05. At the same time S and G2 + M cell percentage of brain and liver cells were significantly decreased.

CONCLUSIONExposure to 50 Hz EMFs may alter cell cycle and induce apoptosis of mouse brain and liver cells.

Animals ; Apoptosis ; radiation effects ; Brain ; cytology ; radiation effects ; Cell Cycle ; radiation effects ; Electromagnetic Fields ; Flow Cytometry ; In Situ Nick-End Labeling ; Liver ; cytology ; radiation effects ; Male ; Mice

OBJECTIVETo assess the effects of tumor necrosis factor-α (TNF-α) in enhancing the radiosensitivity of lung cancer cells in vitro.

METHODSA549 cells were exposed to γ-ray with or without TNF-α treatment. MTT assay was used to evaluate the cell viability, and flow cytometry was performed to assess the cell apoptosis. Western blotting was used to observe the expression of caspase-3 protein in the exposed cells.

RESULTSCompared with the exposed cells without TNF-α treatment, the cells treated with TNF-α showed significantly suppressed cell proliferation, increased the cell apoptosis, altered cell cycle, and increased caspase-3 protein expression after γ-ray exposure.

CONCLUSIONTNF-α can enhance the radiosensitivity of A549 cells to increase the efficiency of radiotherapy with γ-ray irradiation.

Apoptosis ; drug effects ; radiation effects ; Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Gamma Rays ; Humans ; Lung Neoplasms ; Radiation Tolerance ; drug effects ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo investigate the effect of curcumin (Cur) on radiosensitivity of nasopharyngeal carcinoma cell CNE-2 and its mechanism.

METHODThe effect of curcumin on radiosensitivity was determined by the clone formation assay. The cell survival curve was fitted by Graph prism 6. 0. The changes in cell cycle were analyzed by flow cytometry (FCM). The differential expression of long non-coding RNA was detected by gene chip technology. Part of differentially expressed genes was verified by Real-time PCR.

RESULTAfter 10 micro mol L-1 Cur had worked for 24 h, its sensitization enhancement ratio was 1. 03, indicating that low concentration of curcumin could increase the radiosensitivity of nasopharyngeal carcinoma cells; FCM displayed a significant increase of G2 phase cells and significant decrease of S phase cells in the Cur combined radiation group. In the Cur group, the GUCY2GP, H2BFXP, LINC00623 IncRNA were significantly up-regulated and ZRANB2-AS2 LOC100506835, FLJ36000 IncRNA were significantly down-regulated.

CONCLUSIONCur has radiosensitizing effect on human nasopharyngeal carcinoma CNE-2 cells. Its mechanism may be related to the changes in the cell cycle distribution and the expression of long non-coding IncRNA.

Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Curcumin ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; radiation effects ; Humans ; RNA, Long Noncoding ; genetics ; Radiation Tolerance ; drug effects

OBJECTIVETo explore whether microwave radiation may cause injury of primary cultured Sertoli cells.

METHODSThe model of primary cultured Sertoli cells in vitro was established, which was radiated by microwave with average power density 0, 30 and 100 mW/cm(2) for five minutes. The changes of cell cycle, apoptosis and death, and intracellular Ca2+ concentration in the Sertoli cells were measured at sixth hours through Annexin V-PI double labeling and Fluo-3-AM labeling, flow cytometry combined with laser scanning confocal microscopy after microwave exposure.

RESULTSThe numbers of Sertoli cells were obviously reduced in G0-G1 and G2-M phase (62.57% +/- 3.22% and 8.25% +/- 1.75%) and increased in S phase (29.17% +/- 4.87%) compared with the control groups (79.18% +/- 0.24%, 11.17% +/- 0.50% and 9.64% +/- 0.62%) (P < 0.05 or P < 0.01), but the changes of rate of apoptosis and death and intracellular Ca2+ concentration showed no difference at 6 h after exposure to 30 mW/cm(2) microwave. There was a significant increase in the Sertoli cell counts of G0-G1 phase (87.69% +/- 1.32%), and decrease in the Sertoli cell counts of G2-M and S phase (7.41% +/- 0.60% and 4.87% +/- 0.91%) (P < 0.01). There was also a significant increase in intracellular Ca2+ concentration and rate of apoptosis and death (P < 0.05 or P < 0.01) at 6 h after exposure to 100 mW/cm(2) microwave.

CONCLUSION100 mW/cm(2) microwave radiation may cause growth inhibition and increase of apoptosis and death in the primary cultured Sertoli cells. The increase of intracellular Ca2+ concentration is one of the injury mechanisms.

Animals ; Apoptosis ; radiation effects ; Calcium ; metabolism ; Cell Cycle ; radiation effects ; Cells, Cultured ; Male ; Microwaves ; adverse effects ; Rats ; Rats, Wistar ; Sertoli Cells ; metabolism ; pathology ; radiation effects

AIMTo study effect of soybean isoflavones (SI) on spleen in radiated mice.

METHODS90 male mice were randomly divided into control group, radiated group, radiated plus 0.5% dose SI group. After 2-week feeding, the mice received 4.0 Gy 137Cs gamma-radiation, the cell cycles, cell apoptosis and proliferation on the spleen and the spleen index were observed in radiated after 12 h, 24 h, 1 week and 2 weeks.

RESULTSAfter the mice were radiated, the spleen were significantly atrophy, the rate of the cell apoptosis and the cell cycles of G0-G1 phase in splenocytes were significantly increased (P < 0.01), the cell cycles rate of S phase and the proliferation index were significantly decreased in spleen (P < 0.05). Compared with radiated group, the spleen atrophy and the rate of the cell cycles of G0-G1 phase were significantly decreased (P < 0.05), and the cell cycles of G2-M phase and the proliferation index were significantly increased (P < 0.05) in the mice supplied 0.5% soybean isoflavones.

CONCLUSIONThe soybean isoflavones could significantly increase spleen radioprotective effect in mice.

Animals ; Apoptosis ; drug effects ; radiation effects ; Cell Cycle ; drug effects ; radiation effects ; Cellular Structures ; Isoflavones ; pharmacology ; Male ; Mice ; Mice, Inbred Strains ; Radiation, Ionizing ; Soybeans ; Spleen ; cytology