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Mihai, C. T., Rotinberg, P., Brinza, F., & Vochita, G. (2014). Extremely low-frequency electromagnetic fields cause DNA strand breaks in normal cells. Journal of environmental health science & engineering, 12(1), 15.
Abstract: BACKGROUND: Extremely low frequency electromagnetic fields aren't considered as a real carcinogenic agent despite the fact that some studies have showed impairment of the DNA integrity in different cells lines. The aim of this study was evaluation of the late effects of a 100 Hz and 5.6 mT electromagnetic field, applied continuously or discontinuously, on the DNA integrity of Vero cells assessed by alkaline Comet assay and by cell cycle analysis. Normal Vero cells were exposed to extremely low frequency electromagnetic fields (100 Hz, 5.6 mT) for 45 minutes. The Comet assay and cell cycle analysis were performed 48 hours after the treatment. RESULTS: Exposed samples presented an increase of the number of cells with high damaged DNA as compared with non-exposed cells. Quantitative evaluation of the comet assay showed a significantly (<0.001) increase of the tail lengths, of the quantity of DNA in tail and of Olive tail moments, respectively. Cell cycle analysis showed an increase of the frequency of the cells in S phase, proving the occurrence of single strand breaks. The most probable mechanism of induction of the registered effects is the production of different types of reactive oxygen species. CONCLUSIONS: The analysis of the registered comet indices and of cell cycle showed that extremely low frequency electromagnetic field of 100 Hz and 5.6 mT had a genotoxic impact on Vero cells.
Keywords: 5; 6 mt and 100; cell cycle analysis; comet assay; continuous and discontinuous exposure; elf-emf; hz
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Trillo, M. Ã. ., MartÃnez, M. A., Cid, M. A., & Úbeda, A. (2013). Retinoic acid inhibits the cytoproliferative response to weak 50‑Hz magnetic fields in neuroblastoma cells. Oncology reports, 29(3), 885–894.
Abstract: We previously reported that intermittent exposure to a 50‑Hz magnetic field (MF) at 100 µT stimulates cell proliferation in the human neuroblastoma cell line NB69. The present study aimed to investigate whether the magnetic field-induced growth promotion also occurs at a lower magnetic flux density of 10 µT. To this purpose, NB69 cells were subjected for 42 h to intermittent exposure, 3 h on/3 h off, to a 50‑Hz MF at a 10 or 100 µT magnetic flux density. The field exposure took place either in the presence or in the absence of the antiproliferative agent retinoic acid. At the end of the treatment and/or incubation period, the cell growth was estimated by hemocytometric counting and spectrophotometric analysis of total protein and DNA contents. Potential changes in DNA synthesis were also assessed through proliferating cell nuclear antigen (PCNA) immunolabeling. The results confirmed previously reported data that a 42-h exposure to a 50‑Hz sine wave MF at 100 µT promotes cell growth in the NB69 cell line, and showed that 10 µT induces a similar proliferative response. This effect, which was significantly associated and linearly correlated with PCNA expression, was abolished by the presence of retinoic acid in the culture medium.
Keywords: Antineoplastic Agents; Antineoplastic Agents: pharmacology; Cell Line; Cell Proliferation; Cell Proliferation: drug effects; Cell Survival; Cell Survival: drug effects; Humans; Magnetic Fields; Neuroblastoma; Proliferating Cell Nuclear Antigen; Proliferating Cell Nuclear Antigen: metabolism; Tretinoin; Tretinoin: pharmacology; Tumor
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Sheikh, A. Q., Taghian, T., Hemingway, B., Cho, H., Kogan, A. B., & Narmoneva, D. A. (2013). Regulation of endothelial MAPK/ERK signalling and capillary morphogenesis by low-amplitude electric field. Journal of the Royal Society, Interface / the Royal Society, 10(78), 20120548.
Abstract: Low-amplitude electric field (EF) is an important component of wound-healing response and can promote vascular tissue repair; however, the mechanisms of action on endothelium remain unclear. We hypothesized that physiological amplitude EF regulates angiogenic response of microvascular endothelial cells via activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. A custom set-up allowed non-thermal application of EF of high (7.5 GHz) and low (60 Hz) frequency. Cell responses following up to 24 h of EF exposure, including proliferation and apoptosis, capillary morphogenesis, vascular endothelial growth factor (VEGF) expression and MAPK pathways activation were quantified. A db/db mouse model of diabetic wound healing was used for in vivo validation. High-frequency EF enhanced capillary morphogenesis, VEGF release, MEK-cRaf complex formation, MEK and ERK phosphorylation, whereas no MAPK/JNK and MAPK/p38 pathways activation was observed. The endothelial response to EF did not require VEGF binding to VEGFR2 receptor. EF-induced MEK phosphorylation was reversed in the presence of MEK and Ca(2+) inhibitors, reduced by endothelial nitric oxide synthase inhibition, and did not depend on PI3K pathway activation. The results provide evidence for a novel intracellular mechanism for EF regulation of endothelial angiogenic response via frequency-sensitive MAPK/ERK pathway activation, with important implications for EF-based therapies for vascular tissue regeneration.
Keywords: Animals; Apoptosis; Calcium; Calcium: metabolism; Capillaries; Capillaries: cytology; Capillaries: growth & development; Cell Proliferation; Cells; Cultured; Electromagnetic Fields; Extracellular Signal-Regulated MAP Kinases; Extracellular Signal-Regulated MAP Kinases: metabo; Gene Expression Regulation; MAP Kinase Kinase 4; MAP Kinase Kinase 4: metabolism; MAP Kinase Signaling System; Mice; Morphogenesis; Neovascularization; Phosphatidylinositol 3-Kinases; Phosphatidylinositol 3-Kinases: metabolism; Phosphorylation; Physiologic; Proto-Oncogene Proteins c-raf; Proto-Oncogene Proteins c-raf: metabolism; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor A: biosynthesis
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Mo, W. -chuan, Zhang, Z. -jian, Liu, Y., Bartlett, P. F., & He, R. -qiao. (2013). Magnetic shielding accelerates the proliferation of human neuroblastoma cell by promoting G1-phase progression. PloS one, 8(1), e54775.
Abstract: Organisms have been exposed to the geomagnetic field (GMF) throughout evolutionary history. Exposure to the hypomagnetic field (HMF) by deep magnetic shielding has recently been suggested to have a negative effect on the structure and function of the central nervous system, particularly during early development. Although changes in cell growth and differentiation have been observed in the HMF, the effects of the HMF on cell cycle progression still remain unclear. Here we show that continuous HMF exposure significantly increases the proliferation of human neuroblastoma (SH-SY5Y) cells. The acceleration of proliferation results from a forward shift of the cell cycle in G1-phase. The G2/M-phase progression is not affected in the HMF. Our data is the first to demonstrate that the HMF can stimulate the proliferation of SH-SY5Y cells by promoting cell cycle progression in the G1-phase. This provides a novel way to study the mechanism of cells in response to changes of environmental magnetic field including the GMF.
Keywords: Cell Division; Cell Line, Tumor; G1 Phase; G2 Phase; Humans; Magnetic Fields; Neuroblastoma; Neuroblastoma: metabolism; Neuroblastoma: pathology
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Maeda, K., Robinson, A. J., Henbest, K. B., Hogben, H. J., Biskup, T., Ahmad, M., et al. (2012). Magnetically sensitive light-induced reactions in cryptochrome are consistent with its proposed role as a magnetoreceptor. Proceedings of the National Academy of Sciences, 109(13), 4774–4779.
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