Human peripheral blood leukocytes from healthy volunteers have been employed to investigate the induction of genotoxic effects following 2 h exposure to 900 MHz radiofrequency radiation. The GSM signal has been studied at specific absorption rates (SAR) of 0.3 and 1 W/kg. The exposures were carried out in a waveguide system under strictly controlled conditions of both dosimetry and temperature. The same temperature conditions (37.0 +/- 0.1 degrees C) were realized in a second waveguide, employed to perform sham exposures. The induction of DNA damage was evaluated in leukocytes by applying the alkaline single cell gel electrophoresis (SCGE)/comet assay, while structural chromosome aberrations and sister chromatid exchanges were evaluated in lymphocytes stimulated with phytohemagglutinin. Alterations in kinetics of cell proliferation were determined by calculating the mitotic index. Positive controls were also provided by using methyl methanesulfonate (MMS) for comet assay and mitomycin-C (MMC), for chromosome aberration, or sister chromatid exchange tests. No statistically significant differences were detected in exposed samples in comparison with sham exposed ones for all the parameters investigated. On the contrary, the positive controls gave a statistically significant increase in DNA damage in all cases, as expected. Thus the results obtained in our experimental conditions do not support the hypothesis that 900 MHz radiofrequency field exposure induces DNA damage in human peripheral blood leukocytes in this range of SAR.
We studied the DNA isolated from 20 Italian males carryinf haemophilia B using a cDNA probe for factor IX. A large gene deletion was detected in one subject, while the DNA patterns of the other haemophilia B patients were indistinguishable from normal.
Subjects and methodsBlood samples from 20 Italian haemophilia B patients were obtained by standard procedures. DNA preparation and Southern blotting technique were as previously described.'2 DNA was digested with the appropriate restriction enzymes under the conditions indicated by the supplier (Boehringer, Mannheim).Thyroglobulin genomic probe was a generous gift from Dr E Avvedimento.Hybridisation was performed in accordance with the Gene Screen transfer membrane method (New England Nuclear, Boston). Excess probe was washed off by incubation with 0-06 mol/l Tris-HCl (pH 8), 0-3 mol/l NaCl, 0-002 molI EDTA, and 1% SDS at 60°C for one hour, followed by incubation in 0*03 mol/l NaCl, 0-006 mol/l Tris (pH 8), and 0-0002 mol/l EDTA for one hour at room temperature.
We analyzed chromosome aberrations (CAs), sister chromatid exchanges (SCEs), mitotic index (MI), and glucose 6-phosphate dehydrogenase (G6PD) enzyme activity in human peripheral lymphocytes from three healthy donors exposed in vitro to different concentrations of gliphosate, vinclozolin, atrazine, and DPX-E9636. The pesticides gliphosate, vinclozolin, and atrazine have been studied in a broad range of genetic tests with predominantly conflicting or negative results, whereas little is known about the genotoxicity of DPX-E9636. In our experimental conditions, each chemical compound tested produced a dose-related increase in the percent of aberrant cells and an increase of SCE/cell. Furthermore, at the highest concentrations of vinclozolin, atrazine, and DPX-E9636, we observed a significant reduction of the mitotic index. The increase of G6PD activity in exposed lymphocyte cultures strongly indicated an induction of a pro-oxidant state of the cells as an initial response to pesticide exposure.
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