Exposure to radiofrequency radiation emitted from mobile phone jammers adversely affects the quality of human sperm

Background: The health effect of rapidly increasing everyday exposure of humans to radiofrequency radiation is a major global concern. Mobile phone jammers prevent the mobile phones from receiving signals from base stations by interfering with authorized mobile carriers' services. In spite of the fact that mobile jammer use is illegal, they are occasionally used in offices, shrines, conference rooms and cinemas. The purpose of this study was to investigate the biological effects of short term exposure of human sperm to radiofrequency radiation emitted from a commercial mobile phone jammer

Materials and Methods: Fresh semen samples were obtained by masturbation from 50 healthy donors who had referred with their wives to Infertility Treatment Center at the Mother and Child Hospital, Shiraz University of Medical Sciences. Female problem was diagnosed as the reason for infertility in these couples. The semen sample of each participant was divided into 4 aliquots. The first aliquot was subjected to swim-up and exposed to jammer radiation. The second aliquot was not subjected to swim-up but was exposed to jammer radiation. The third and fourth aliquots were not exposed to jammer radiation but only the 3rd aliquot was subjected to swim-up

Results: Semen samples exposed to radiofrequency radiation showed a significant decrease in sperm motility and increase in DNA fragmentation

Conclusion: Electromagnetic radiation in radiofrequency range emitted from mobile phone jammers may lead to decreased motility and increased DNA fragmentation in human semen. It can be concluded that mobile phone jamming might exert adverse reproductive health effects

Low energy proton beam induces tumor cell apoptosis through reactive oxygen species and activation of caspases

Proton beam is useful to target tumor tissue sparing normal cells by allowing precise dose only into tumor cells. However, the cellular and molecular mechanisms by which proton beam induces tumor cell death are still undefined. We irradiated three different tumor cells (LLC, HepG2, and Molt-4) with low energy proton beam (35 MeV) with spread out Bragg peak (SOBP) in vitro, and investigated cell death by MTT or CCK-8 assay at 24 h after irradiation. LLC and HepG2 cells were sensitive to proton beam at over 10 Gy to induce apoptosis whereas Molt-4 showed rather low sensitivity. Relative biological effectiveness (RBE) values for the death rate relative to gamma-ray were ranged from 1.1 to 2.3 in LLC and HepG2 but from 0.3 to 0.7 in Molt-4 at 11 d after irradiation by colony formation assay. The typical apoptotic nuclear DNA morphological pattern was observed by staining with 4'-6-diamidino-2-phenylindole (DAPI). Tiny fragmented DNA was observed in HepG2 but not in Molt-4 by the treatment of proton in apoptotic DNA fragment assay. By FACS analysis after stained with FITC-Annexin-V, early as well as median apoptotic fractions were clearly increased by proton treatment. Proton beam-irradiated tumor cells induced a cleavage of poly (ADP-ribose) polymerase-1 (PARP-1) and procaspases-3 and -9. Activity of caspases was highly enhanced after proton beam irradiation. Reactive oxygen species (ROS) were significantly increased and N-acetyl cysteine pretreatment restored the apoptotic cell death induced by proton beam. Furthermore, p38 and JNK but not ERK were activated by proton and dominant negative mutants of p38 and JNK revived proton-induced apoptosis, suggesting that p38 and JNK pathway may be activated through ROS to activate apoptosis. In conclusion, our data clearly showed that single treatment of low energy proton beam with SOBP increased ROS and induced cell death of solid tumor cells (LLC and HepG2) in an apoptotic cell death program by the induction of caspases activities.