OBJECTIVETo explore the impact of microwave radiation on GC-2spd cells.

METHODSWe exposed cultured GC-2spd cells to microwave radiation at the average power densities of 0, 10 and 30 mW/cm2 for 15 minutes and, from I to 24 hours after the exposure, we observed the changes in cell proliferation, histology and ultrastructure, cell apoptosis, and cAMP content by MTIT, light microscopy, electron microscopy, flow cytometry and ELISA.

RESULTSCompared with the control group, the GC-2spd cells showed a significant decrease in proliferation ability at 1 -24 hours after 10 and 30 mW/cm2 microwave radiation, except at 12 hours after 30 mW/cm2 radiation (P <0.05 or P <0.01), with reduced length and number of cell enation and increased intra cytoplasm vacuoles. The rate of cell apoptosis (%) was significantly increased in the 10 and 30 mW/cm2 groups at 6 hours (4.56 +/- 2.09 vs 14.59 +/- 1.09 and 8.48 +/- 1.73, P <0.05 or P <0.01) , with agglutination and margin translocation of chromatins and obvious dilation of endo cytoplasmic reticula. The cAMP content (nmol/g) in the GC-2spd cells was remarkably reduced in the 10 and 30 mW/cm2 groups at 6 and 24 hours (2.77 +/-0.24 vs 1.65+/- 0. 17 and 1.96+/-0.10, 3.02 +/-0.47 vs 2.13 +/-0.33 and 1.69 +/-0.27, P <0.05 or P <0.01).

CONCLUSIONMicrowave radiation at 10 and 30 mW/cm2 may cause injury to GC-2spd cells, which is manifested by decreased content of intracellular cAMP, reduced activity of cell proliferation, and increased rate of cell apoptosis.

Animals ; Apoptosis ; radiation effects ; Cell Line ; radiation effects ; Cell Proliferation ; radiation effects ; Male ; Mice ; Microwaves ; adverse effects ; Spermatocytes ; radiation effects

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

The study examined the role of endoplasmic reticulum stress (ERS) and signaling pathways of inositol-requiring enzyme-1 (IRE1), RNA-activated protein kinase-like ER kinase (PERK) and activating transcription factor-6 (ATF6) in apoptosis of mouse testicular cells treated with low-dose radiation (LDR). In the dose-dependent experiment, the mice were treated with whole-body X-ray irradiation at different doses (25, 50, 75, 100 or 200 mGy) and sacrificed 12 h later. In the time-dependent experiment, the mice were exposed to 75 mGy X-ray irradiation and killed at different time points (3, 6, 12, 18 or 24 h). Testicular cells were harvested for experiments. H(2)O(2) and NO concentrations, and Ca(2+)-ATPase activity were detected by biochemical assays, the calcium ion concentration ([Ca(2+)]i) by flow cytometry using fluo-3 probe, and GRP78 mRNA and protein expressions by quantitative real-time RT-PCR (qRT-PCR) and Western blotting, respectively. The mRNA expressions of S-XBP1, JNK, caspase-12 and CHOP were measured by qRT-PCR, and the protein expressions of IRE1α, S-XBP1, p-PERK, p-eIF2α, ATF6 p50, p-JNK, pro-caspase-12, cleaved caspase-12 and CHOP by Western blotting. The results showed that the concentrations of H2O2 and NO, the mRNA expressions of GRP78, S-XBP1, JNK, caspase-12 and CHOP, and the protein expressions of GRP78, S-XBP1, IRE1α, p-PERK, p-eIF2α, ATF6 p50, p-JNK, pro-caspase-12, cleaved caspase-12 and CHOP were significantly increased in a time- and dose-dependent manner after LDR. But the [Ca(2+)]i and Ca(2+)-ATPase activities were significantly decreased in a time- and dose-dependent manner. It was concluded that the ERS, regulated by IRE1, PERK and ATF6 pathways, is involved in the apoptosis of testicular cells in LDR mice, which is associated with ERS-apoptotic signaling molecules of JNK, caspase-12 and CHOP.
Animals ; Apoptosis ; physiology ; radiation effects ; Endoplasmic Reticulum Stress ; physiology ; radiation effects ; Male ; Mice ; Radiation ; Testis ; physiology ; radiation effects

Animals ; Apoptosis ; radiation effects ; Electromagnetic Fields ; adverse effects ; Hippocampus ; pathology ; radiation effects ; Male ; Maze Learning ; radiation effects ; Rats ; Rats, Wistar

More and more evidence from over 50 years of researches on the effects of electromagnetic radiation on male reproduction show that a certain dose of electromagnetic radiation obviously damages male reproduction, particularly the structure and function of spermatogenic cells. The mechanisms of the injury may be associated with energy dysmetabolism, lipid peroxidation, abnormal expressions of apoptosis-related genes and proteins, and DNA damage.
Animals ; Apoptosis Regulatory Proteins ; metabolism ; DNA Damage ; radiation effects ; Dose-Response Relationship, Radiation ; Electromagnetic Radiation ; Energy Metabolism ; radiation effects ; Genitalia, Male ; radiation effects ; Lipid Peroxidation ; radiation effects ; Male ; Radiation, Ionizing ; Reproduction ; radiation effects

OBJECTIVETo study the effect of high power microwave (HPM) radiation on the testicular germ cell apoptosis.

METHODSOne hundred and twenty-five Spraque-Dawley rats were randomly divided into two groups, unexposed control group and experimental group(further divided into four subgroups: 10 mW/cm2 5 min, 10 mW/cm2 10 min, 20 mw/cm2 5 min, and 20 mW/cm2 10 min), and then the experimental group was radiated with S wave band of 10 mW/cm2, 20 mW/cm2 high power microwave for 5 or 10 min. Testicular samples were taken at 6 h, 24 h, 48 h, 72 h and 5 d after radiation and separately studied. At the end of the process, testicular germ cell apoptosis was detected by in situ terminal deoxynucleotityl transferase mediated dUTP nick end labeling (TUNEL).

RESULTSThe number of apoptotic cells of the 6 h, 24 h and 48 h experimental groups at 5 min after 10 and 20 mW/cm2 radiation was remarkably larger than that of the controls (P < 0.01), especially after 10 mW/cm2 radiation, the number of the 6 h group reached the peak (161.27 +/- 5.90) /5 convoluted seminiferous tubules. The changes in the other experimental groups had no significant difference compared with the controls (P > 0.05).

CONCLUSIONHPM can increase germ cell apoptosis of the rat testis, which is related to the time of radiation and sample acquisition. In the condition of the present test, 5 minutes of HPM radiation may significantly enhance testicular germ cell apoptosis and damage, which in turn may influence the reproductive function of the rats.

Animals ; Apoptosis ; radiation effects ; Male ; Microwaves ; Rats ; Rats, Sprague-Dawley ; Spermatozoa ; pathology ; radiation effects ; Testis ; radiation effects

ObjectiveTo investigate the influence of cellphone electromagnetic radiation (CER) on the testicular ultrastructure and the apoptosis of spermatogenic cells in male rats.atability, feasibility, applicability, and controllability in the construction of experimental animal models, we compared the major anatomic features of the penis of 20 adult beagle dogs with those of 10 adult men. Using microsurgical techniques, we performed cross-transplantation of the penis in the 20 (10 pairs) beagle dogs and observed the survival rate of the transplanted penises by FK506+MMF+MP immune induction. We compared the relevant indexes with those of the 10 cases of microsurgical replantation of the amputated penis.

METHODSThirty adult male SD rats were equally randomized into a 2 h CER, a 4 h CER, and a normal control group, the former two groups exposed to 30 days of 900 MHz CER for 2 and 4 hours a day, respectively, while the latter left untreated. Then the changes in the ultrastructure of the testis tissue were observed under the transmission electron microscope and the apoptosis of the spermatogenic cells was determined by TUNEL.

RESULTSCompared with the normal controls, the rats of the 2 h CER group showed swollen basement membrane of seminiferous tubules, separated tight junction of Sertoli cells, increased cell intervals, apparent vacuoles and medullization in some mitochondria, and increased apoptosis of spermatogenic cells, mainly the apoptosis of primary spermatocytes (P<0.05 ). In comparison with the 2 h CER group, the animals of the 4 h CER group exhibited swollen basement membrane of seminiferous tubules, more separated tight junction of Sertoli cells, wider cell intervals, incomplete membrane of spermatogonial cells, fragments of cytoplasm, nuclear pyknosis and notch, slight dilation of perinuclear space, abnormalities of intracellular mitochondria with vacuoles, fuzzy structure, and fusion or disappearance of some cristae, and increased damage of mitochondria and apoptosis of spermatogenic cells, including the apoptosis of spermatogonial cells, primary spermatocytes, and secondary spermatocytes (P<0.05 ).

CONCLUSIONSCER can damage the testicular ultrastructure and increase the apoptosis of spermatogenic cells of the male rat in a time-dependent manner, and the apoptosis of spermatogenic cells may be associated with the damage to mitochondria.

Animals ; Apoptosis ; Cell Phone ; Electromagnetic Radiation ; Male ; Mitochondria ; radiation effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Seminiferous Tubules ; radiation effects ; Sertoli Cells ; radiation effects ; Spermatocytes ; radiation effects ; Spermatogonia ; radiation effects ; Testis ; radiation effects ; ultrastructure

OBJECTIVETo investigate the effects of microwave radiation on thymocytes in mice at different power densities.

METHODSThe experimental animals were whole-body exposed to microwave radiation with frequency of 2,450 MHz, power density of 1, 5, 15 mW/cm(2) respectively 1 h everyday for 30 days. Then the thymus were taken out after the mice were decapitated. Thymus index, morphological characteristics of thymus were examined. The changes of thymus T-cell subgroups, cell cycle progression in thymocytes and cellular apoptosis were detected with flow cytometry (FCM).

RESULTSThe body weights of animals in 5, 15 mW/cm(2) irradiation groups [(28.10 +/- 1.46), (27.50 +/- 2.52) g] were lower than that of the control [(31.95 +/- 2.51) g] (P < 0.05). Pathological observation showed dark red piece of nucleus, some nuclei inclined to one side, slight increase in hassall body. The expressions of CD8 in 5, 15 mW/cm(2) irradiation groups (29.14% +/- 1.68%, 29.18% +/- 0.81%) were higher than that in control group (26.95% +/- 1.27%) (P < 0.05). The percentages of G(2) + M phase thymocytes in both radiation groups (12.24% +/- 1.82%, 11.19% +/- 1.36%) were lower than that in control group (14.58% +/- 0.64%) (P < 0.01). Thymocytic apoptosis rates in the three experimental groups (7.18% +/- 0.99%, 10.06% +/- 1.58%, 9.45% +/- 0.92%) were higher than that in control (4.25% +/- 1.63%) (P < 0.01), but the evident difference between 5 mW/cm(2) and 15 mW/cm(2) was not found (P > 0.05).

CONCLUSIONSub-chronic microwave exposure (2 450 MHz, 5, 15 mW/cm(2)) could induce thymocyte apoptosis, cause pathological changes in thymus, and affect cell cycle progression, thus may inhibit the immune function of the animal.

Animals ; Apoptosis ; radiation effects ; Dose-Response Relationship, Radiation ; Female ; Male ; Mice ; Microwaves ; adverse effects ; T-Lymphocytes ; radiation effects ; Thymus Gland ; cytology ; 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