Since discovery of X-rays, radiotherapy has evolved into one of the most scientific branches of medicine and has established its role as the primary line or the secondary line of attack, after surgery,. in the treatment of malignant cancers. Nowadays its importance is illustrated by the fact that as many as 70 per cent of all pastients with cancer will receive radiation therapy at sometime during their disease process. Biologic effects-of X-rays began to be apparant soon after the discovery by Roentgen in 1895. In clinical radiotherapy, the biologic endpoint of most importance is loss of cellular reproductive ability or clonogenicity. One of the commonest ;nays to assess cell survival is to use an in vitro plating assay. We analyzed radiation effect on colony formation of HaLa. S3(SC) cell line and obtained results are as follows The plating efficiency is 0.464. The shape of cell survival curve is similar to multi-target plus single hit component model. Estimated values of Do, Dq, and extrapolation number are 150 cGy, 80 cGy and 1.7 respectively. We reported these experimental data with review of literature.
Cell Line* ; Cell Survival ; Radiation Effects ; Radiotherapy

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

The purpose of this study is to investigate the mechanism of alternative responses to low dose irradiation for neuronal cell proliferation in the dentate gyrus of rats. To determine the effect of a single exposure to radiation, rats were irradiated with a single dose of 0.1, 1, 10 or 20 Gy. To determine the effect of the cumulative dose, the animals were irradiated daily with 0.01 Gy or 0.1 Gy from 1 to 4 days. The neuronal cell proliferation was evaluated using immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), Ki-67 and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Four consecutive daily irradiations with a 0.01 Gy/fraction increased the number of BrdU-positive and Ki-67-positive cells in a dose dependent manner, but this did not affect the number of TUNEL-positive cells. However, there was not a dose dependent relationship for the 0.1 Gy/fraction irradiation with the number of BrdU, Ki-67 and TUNEL positive cells. Our data support the explanation that the adaptive response, induced by low-dose radiation, in the hippocampus of rats is more likely a reflection of the perturbations of cell cycle progression.
Rats, Sprague-Dawley ; Rats ; Radiation Dosage ; Neurons/*cytology/*radiation effects ; Neuronal Plasticity/*radiation effects ; Male ; Dose-Response Relationship, Radiation ; Dentate Gyrus/*cytology/*radiation effects ; Cell Survival/radiation effects ; Cell Proliferation/*drug effects ; Animals ; Adaptation, Physiological/radiation effects

The effect of local hyperthermia of 41 to 43degree C for 30 minutes on radiosensitivity of normal tissue was studied utilizing jejunal crypt microcolony assay. Hyperthermia of this range enhanced the radiation effect and the effect was mainly additive without significant effect on the slopes of cell survival curves. At the isoeffect level of 20 microcolony formation, the thermal enhancement ratio was 1.02, 1.10 and 1.39 for 41degree 42degreeand 43degree C, respectively. The distribution of microcolony formation along the circumference of jejunum was not uniform, having more colonies around the mesenteric border, and this suggests the effect of uneven cooling by blood circulation.
Animals ; Blood Circulation ; Cell Survival ; Fever* ; Hyperthermia, Induced ; Jejunum* ; Mice* ; Radiation Effects ; Radiation Tolerance

OBJECTIVETo investigate the biological effects of ultraviolet B (UVB) irradiation on human bronchial epithelial cells (16HBE cells) and explore the possible mechanism.

METHODSThe survival rates of 16HBE cells were detected by MTT assay at 12 h after UVB irradiation at different doses (0, 10, 30, 50, 70, and 100 J/m(2)) or at 50 J/m(2) for different durations (2, 4, 8, 12, and 24 h). The DNA ladder was detected by agarose gel electrophoresis, the cell cycle changes were analyzed by flow cytometry, and the expression of nuclear factor-κB (NF-κB)/p65 protein was assayed by Western blotting following the exposures.

RESULTSUVB irradiation of the cells resulted in lowered cell survival rates, DNA fragmentation, S phase arrest and up-regulation of NF-κB/p65 protein expression.

CONCLUSIONSUVB irradiation can induce growth inhibition and apoptosis of 16HBE cells, in which process NF-κB protein may play a key role.

Apoptosis ; radiation effects ; Bronchi ; cytology ; Cell Line ; Cell Survival ; radiation effects ; Endothelial Cells ; cytology ; radiation effects ; Humans ; NF-kappa B ; metabolism ; Ultraviolet Rays ; adverse effects

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

Cryptosporidium parvum is a well-known waterborne and opportunistic intracellular protozoan parasite that causes diarrheal illness. In this study, we quantitatively investigated reduction of the infectivity of C. parvum after gamma irradiation and repair of the infectivity during incubation time after irradiation. C. parvum oocysts were subjected to gamma irradiation at various doses (1, 5, 10, and 25 kGy), and the in vitro infectivity was measured by real-time PCR every day up to 7 days after irradiation. The in vitro infectivity of C. parvum on human ileocecal adenocarcinoma cells (HCT-8) was effectively reduced (> 2 log(10)) by irradiation at 10 kGy or more. However, in the experiment to find out repair of the infectivity, recovery was not noted until day 7 post-incubation.
Animals ; Cell Line, Tumor ; Cell Survival/radiation effects ; Cryptosporidiosis/*parasitology ; Cryptosporidium parvum/genetics/*pathogenicity/*radiation effects ; Female ; *Gamma Rays ; Humans ; Mice ; Mice, Inbred C57BL ; Oocysts/radiation effects ; Virulence

OBJECTIVETo explore the effect of NAD+ against radiation injury and its dose-effect relationship.

METHODSL02 liver cells cultured in RPMI 1640 medium containing 10% fetal calf serum were exposed to X-ray irradiation followed by immediate application of NAD+. The cellular viability was analyzed by MTT assay and the apoptotic cells were detected by TUNEL methods to observe the damages of L02 liver cells induced by X-ray exposure and analyze the dose-effect relationship of NAD+.

RESULTSThe viability of L02 liver cells was decreased with increasing dose of X-ray irradiation. The most obvious growth inhibition of L02 cells occurred 24 h after the irradiation. NAD+ significantly increased the cell survival rate after irradiation, and this effect was gradually increased within the concentration range of 100-1000 microg/ml; at higher concentrations, the survival rate of the irradiated L02 cells showed no significant increase.

CONCLUSIONNAD+ provides partial protection of the liver cells against radiation injury, and the effect is positively correlated to NAD+ concentration within a certain range.

Apoptosis ; drug effects ; radiation effects ; Cell Line ; Cell Survival ; drug effects ; radiation effects ; Dose-Response Relationship, Drug ; Hepatocytes ; cytology ; drug effects ; radiation effects ; Humans ; NAD ; administration & dosage ; pharmacology ; Radiation Injuries ; prevention & control

OBJECTIVETo explore the relationship between DNA repair in vitro and in vivo after irradiation, and to describe the curves of DNA repair which can improve the accuracy of radiation dose estimation.

METHODSThe DNA double-strand break in lymphocytes of human and mouse was detected using neutral single cell gel electrophoresis (SCGE) after radiation and the curves of DNA repair individually were estimated, which were compared later.

RESULTSAlong with the time lapsing, the DNA repair of human peripheral blood and mice increased significantly and the residual damage decreased gradually, which showed significant time-effect relationship. The curve of DNA repair in vitro of human lymphocytes presented the same log model as that of mouse DNA repair in vivo. The curve showed as followed respectively: Mice: Y(TM) = 55.8256 - 10.792 lnX (R(2) = 0.629, P < 0.01) and Y(OTM) = 25.4173 - 4.5273 lnX (R(2) = 0.661, P < 0.01); Human: Y(TM) = 30.242 7 - 7.383 6 lnX (R(2) = 0.686, P < 0.01) and Y(OTM) = 17.9772 - 3.9125 lnX (R(2) = 0.752, P < 0.01).

CONCLUSIONThe curve of DNA repair in vitro of human lymphocytes could be considered in biodosimetry estimation because the process of DNA repair in vitro could display the repair level and speed of DNA double-strand break in vivo.

Animals ; Cell Survival ; Comet Assay ; DNA Damage ; radiation effects ; DNA Repair ; radiation effects ; Dose-Response Relationship, Radiation ; Female ; Humans ; Lymphocytes ; radiation effects ; Male ; Mice ; Mice, Inbred Strains ; Radiation Dosage ; Single-Cell Analysis

Ascaris suum eggs are inactivated by composting conditions; however, it is difficult to find functional changes in heat-treated A. suum eggs. Here, unembryonated A. suum eggs were incubated at 20degrees C, 50degrees C, and 70degrees C in vitro, and the gene expression levels related to viability, such as eukaryotic translation initiation factor 4E (IF4E), phosphofructokinase 1 (PFK1), and thioredoxin 1 (TRX1), and to apoptosis, such as apoptosis-inducing factor 1 (AIF1) and cell death protein 6 (CDP6), were evaluated by real-time quantitative RT-PCR. No prominent morphological alterations were noted in the eggs at 20degrees C until day 10. In contrast, the eggs developed rapidly, and embryonated eggs and hatched larvae began to die, starting on day 2 at 50degrees C and day 1 at 70degrees C. At 20degrees C, IF4E, PFK1, and TRX1 mRNA expression was significantly increased from days 2-4; however, AIF1 and CDP6 mRNA expression was not changed significantly. IF4E, PFK1, and TRX1 mRNA expression was markedly decreased from day 2 at 50degrees C and 70degrees C, whereas AIF1 and CDP6 mRNA expression was significantly increased. The expressions of HSP70 and HSP90 were detected for 9-10 days at 20degrees C, for 3-5 days at 50degrees C, and for 2 days at 70degrees C. Taken together, incremental heat increases were associated with the rapid development of A. suum eggs, decreased expression of genes related to viability, and earlier expression of apoptosis-related genes, and finally these changes of viability- and apoptosis-related genes of A. suum eggs were associated with survival of the eggs under temperature stress.
Animals ; *Apoptosis ; Ascaris suum/*genetics/*radiation effects ; Cell Survival/radiation effects ; Eggs/radiation effects ; Female ; Gene Expression Profiling ; Gene Expression Regulation/*radiation effects ; Real-Time Polymerase Chain Reaction ; Survival Analysis ; Temperature