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Single Cell Gel Electrophoresis (single + cell_gel_electrophoresis)
Kinds of Single Cell Gel Electrophoresis Selected AbstractsEvaluation of systemic oxidative status and mononuclear leukocytes DNA damage in children with caustic esophageal strictureDISEASES OF THE ESOPHAGUS, Issue 4 2006M. Kaya SUMMARY., Esophageal stricture (ES) due to accidentally caustic digestions is a common problem in children. Mucosal damage and repeated dilatations lead to chronic inflammation and finally ES. We investigated the oxidative status and DNA damage of children with ES. Five children with ES were compared with the same age- and sex-matched healthy subjects. Oxidative status of plasma was evaluated by measuring myeloperoxidase (MPO) activity, and total peroxide (TP) level. Anti-oxidative status of the plasma was evaluated by measuring catalase (CAT) activity, and total antioxidant response (TAR). We used the Single Cell Gel Electrophoresis (also called Comet Assay) to measure DNA strand break in peripheral blood mononuclear leukocytes. Mean MPO activity and TP levels in the ES group were significantly higher than the control group (0.83 ± 0.35, 0.09 ± 0.03 and 0.98 ± 0.38, 0.34 ± 0.20, P = 0.009 and P = 0.047 respectively). There was no significant difference in CAT activity and TAR levels between the two groups (P = 0.347). DNA damage in patients with ES was increased compared to control subjects (108.8 ± 51.2 and 57.6 ± 31.2 arbitrary units, respectively), but this difference was not significant statistically (P= 0.09). This study shows that systemic oxidative stress and alteration at the nuclear level occur in patients with ES, as a result of multiple dilatations and tissue injury. On the other hand, these results support that patients with ES may benefit from antioxidant treatment. [source] DNA damage in peripheral blood leukocytes of physically active individuals as measured by the alkaline single cell gel electrophoresis assayENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 4 2009Gursatej Gandhi Abstract DNA damage induced by physical activity and/or exercise has been reported under different conditions but not for individuals maintaining physical fitness by regular strenuous exercise. Therefore, we compared levels of DNA damage in blood leukocytes of 40 healthy individuals (35 males, 5 females) who regularly exercised in gymnasiums/health clubs and 15 healthy sedentary controls who had never exercised. The former group was selected (after informed consent) on the basis of how long they had been exercising on a regular basis as well as their exercise schedule and regimen. The length of time since starting a regular exercise regimen ranged from 2 months to 9 years, whereas the daily exercise duration ranged from 40 min to 3 hrs and warm-up sessions ranged from none to 90 min. The length of DNA migration (44.66 ± 2.68 ,m in males, 29.62 ± 1.69 ,m in females) and the percentage of cells with tails (79.86 ±1.27% in males, 67.20 ± 0.96% in females) in peripheral blood leukocytes of physically active individuals were increased significantly (P < 0.001) with respect to corresponding values in control males and females (18.85 ± 1.79 ,m, 23.37 ± 3.94 ,m; 24.50 ± 1.98%, 33.00 ± 4.44%, respectively). Highly significant differences for DNA damage were also observed between physically active males and females. These observations, in the absence of any other exposures, indicate a correlation between strenuous exercise to keep fit and increased levels of DNA damage. This finding may have relevance in terms of the ageing process, with diseases associated with aging, and with carcinogenesis. Environ. Mal. Mutagen. 2009. © 2009 Wiley-Liss, Inc. [source] Three structurally homologous isothiocyanates exert "Janus" characteristics in human HepG2 cellsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2009Evelyn Lamy Abstract In this study, we used the single cell gel electrophoresis (SCGE) assay and the micronucleus (MN) test to investigate the DNA damaging effects and the antigenotoxic potencies of three structurally related ITCs in human HepG2 cells. The results show that all three ITCs possess the characteristic of a "Janus" compound, i.e., they exert both significant genotoxicity and antigenotoxicity, depending on the concentrations used in the test systems applied. Regression line analysis of the results derived by SCGE analysis showed genotoxic potency of the ITCs in the following order: 3-methylthiopropyl ITC (MTPITC) > 4-methylthiobutyl ITC (MTBITC) > 5-methylthiopentyl ITC (MTPeITC); however, this order in genotoxic potency was not confirmed by MN analysis. Additionally, the MN test showed significant mutagenicity of the test substances at higher concentrations when compared with the SCGE assay. Twenty-four hour-treatment of the cells with the ITCs, followed by a 1-hr recovery period, showed significant DNA repair in the SCGE assay at a concentration ,10 ,M MTPITC, ,3 ,M MTBITC, and ,0.1 ,M MTPeITC, respectively. In antigenotoxicity studies, the most effective concentration of MTPITC and MTPeITC toward B(a)P-induced DNA damage was 0.1 ,M in both test systems. MTBITC suppressed MN formation in B(a)P-treated cells to the background level at a concentration of 1 ,M. The ambivalent character of the ITCs under studymust be further clarified, especially in the possiblecontext of high dose therapeutic applications. Environ. Mol. Mutagen. 2009. © 2009 Wiley-Liss, Inc. [source] Chlorpyrifos-induced DNA damage in rat liver and brainENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 6 2008Anugya Mehta Abstract Chlorpyrifos (O,O'-diethyl- O -3,5,6-trichloro-2-pyridyl phosphorothionate, CPF) is a broad spectrum organophosphate pesticide used to control a variety of pests. The present study was undertaken to test the in vivo genotoxic potential of CPF in rats, using the single cell gel electrophoresis (or comet) assay. The rats were administered 50 mg and 100 mg CPF/kg body weight daily for 1, 2, and 3 days as well as 1.12 mg and 2.24 mg CPF/kg body weight for 90 days. The level of DNA damage was estimated by scoring 100 cells per animal, dividing into five types: types 0, I, II, III, and IV. The results clearly indicate that exposure to CPF, acutely or chronically, caused a dose-dependent increase in DNA damage in the liver and brain of rats. From the present study, it can be concluded that CPF exhibits genotoxic potential in vivo. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. [source] Influence of the SCGE protocol on the amount of basal DNA damage detected in the Mediterranean mussel, Mytilus galloprovincialisENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 8 2006Nicola Machella Abstract Genotoxicity studies using the single cell gel electrophoresis (SCGE) assay indicate that basal levels of DNA strand breaks (SBs) in marine invertebrates are higher and more variable than those in marine vertebrates. This elevated level of DNA damage was attributed to a large number of alkali-labile sites, which are characteristic of the tightly-packaged DNA in invertebrate cells. To investigate if altering the SCGE protocol can artificially modulate high levels of SBs, SCGE experiments were performed on haemocytes from the Mediterranean mussel (Mytilus galloprovincialis) using proteinase K (PK) digestion in combination with assay buffers containing various concentrations of EDTA. In addition, the effects of Trolox® (soluble antioxidant) and aurintricarboxylic acid (ATA; inhibitor of Ca2+/Mg2+ -dependent nucleases) also were tested. The levels of SBs in M. galloprovicialis cells were compared with SBs in cells from a terrestrial mollusk (the snail Helix aspersa), and a teleost fish (the seabass Dicentrarchus labrax). The integrity of M. galloprovincialis DNA isolated with phenol extractions using EDTA, Trolox, and ATA was further assayed by gel electrophoresis. High SBs in mussel cells were reduced by combining EDTA with PK digestion, or using Trolox® or ATA during cell processing for the SCGE assay. Snails and seabass had lower levels of SBs in the SCGE assay, and the levels were not affected by the protocol modifications. Adding EDTA, Trolox®, or ATA to phenol extractions of M. galloprovincialis genomic DNA also reduced the extent of DNA fragmentation. These results suggest that the internal fluids of M. galloprovincialis may increase the basal levels of DNA SBs through oxidative and/or enzyme-mediated pathways. M. galloprovincialis is used extensively as a sentinel species for assessing the genotoxic hazard of marine pollutants. Our data suggest that the SCGE protocol should be carefully considered when assessing DNA damage in these species. Environ. Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source] DNA damage in Pakistani pesticide-manufacturing workers assayed using the Comet assayENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 8 2006Javed A. Bhalli Abstract The production and use of chemical pesticides has increased in recent years. Although the increased use of pesticides may benefit agriculture, they are also the potential source of environmental pollution, and exposure to pesticides can have negative consequences for human health. In the present study, we have assessed DNA damage in blood leukocytes from 29 Pakistani pesticide-factory workers and 35 controls of similar age and smoking history. The workers were exposed to various mixtures of organophosphates, carbamates, and pyrethroids. DNA damage was measured with the single cell gel electrophoresis (SCGE) assay or Comet assay, using the mean comet tail length (,m) as the DNA damage metric. Exposed workers had significantly longer comet tail lengths than the controls (mean ± SD 19.98 ± 2.87 vs. 7.38 ± 1.48, P < 0.001). Of the possible confounding factors, smokers had significantly longer mean comet tail lengths than nonsmokers and exsmokers for both the workers (21.48 ± 2.58 vs.18.37 ± 2.28, P < 0.001) and the controls (8.86 ± 0.56 vs. 6.79 ± 1.31, P < 0.001), while age had a minimal effect on DNA damage (P > 0.05 and P < 0.05 for workers and controls, respectively). The results of this study indicate that occupational exposure to pesticides causes DNA damage. Environ. Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source] Relationships between cagA, vacA, and iceA genotypes of Helicobacter pylori and DNA damage in the gastric mucosaENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2004Marcelo S.P. Ladeira Abstract Helicobacter pylori (H. pylori) is believed to predispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA. In this study, we investigated the relationships between DNA damage in the gastric mucosa and cagA, vacA, and iceA genotypes of H. pylori. The study was conducted with biopsies from the gastric antrum and corpus of 98 H. pylori -infected and 26 uninfected control patients. H. pylori genotypes were determined by PCR and DNA damage was measured in gastric mucosal cells by the Comet assay (single cell gel electrophoresis). All patients were nonsmokers, not abusing alcohol, and not using prescription or recreational drugs. Levels of DNA damage were significantly higher (P < 0.0001) in the H. pylori -infected patients than in uninfected patients. In comparison with the level of DNA damage in the uninfected controls, the extent of DNA damage in both the antrum (OR = 8.45; 95% CI = 2.33,37.72) and the corpus (OR = 6.55; 95% CI = 2.52,17.72) was related to infection by cagA+/vacAs1m1 and iceA1 strains. The results indicate that the genotype of H. pylori is related to the amount of DNA damage in the gastric mucosa. These genotypes could serve as biomarkers for the risk of extensive DNA damage and possibly gastric cancer. Environ. Mol. Mutagen. 44:91,98, 2004. © 2004 Wiley-Liss, Inc. [source] Subchronic organismal toxicity, cytotoxicity, genotoxicity, and feeding response of pacific oyster (Crassostrea gigas) to lindane (,-HCH) exposure under experimental conditionsENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 10 2007Gerardo Anguiano Abstract This study evaluated organismal toxicity, cytotoxicity, and genotoxicity and the filtration rate in response to different concentrations of subchronic lindane (gamma-hexachlorocyclohexane [,-HCH]), exposure (12 d) in adult Pacific oysters Crassostrea gigas. Oysters were exposed in vivo in laboratory aquaria to 10 different concentrations (0.0,10.0 mg/L) of ,-HCH. The median lethal concentration (LC50) after 12 d was calculated as 2.22 mg/L. Cytotoxic effects were observed in hemocytes, where the mean cell viability was significantly decreased at 1.0 mg/L of ,-HCH after 12 d. Genotoxicity of ,-HCH measured by single cell gel electrophoresis assay, in hemocytes was evident at 0.7 mg/L of ,-HCH after 12 d. After 4 h of exposure to ,-HCH, filtration rates were reduced compared with controls to 65.8 and 38.2% at concentrations of 0.3 and 0.7 mg/L, respectively, and after 11 d of exposure, filtration rates were reduced to 60.4 and 30.9% at concentrations of 0.1 mg/L and higher. These results show the subchronic effects of ,-HCH at different concentrations and effect sensitivities are categorized as filtration rate < genotoxicity < cytotoxicity < mortality. The relevance of integral toxicity evaluation, considering different endpoints from molecular, cellular, and individual levels is discussed. [source] The Effect of Helicobacter pylori Infection on Levels of DNA Damage in Gastric Epithelial CellsHELICOBACTER, Issue 5 2002S. M. Everett Abstract Background.Helicobacter pylori infection leads to an increased risk of developing gastric cancer. The mechanism through which this occurs is not known. We aimed to determine the effect of H. pylori and gastritis on levels of DNA damage in gastric epithelial cells. Methods. Epithelial cells were isolated from antral biopsies from 111 patients. DNA damage was determined using single cell gel electrophoresis and the proportion of cells with damage calculated before and 6 weeks after eradication of H. pylori. Cell suspensions generated by sequential digestions of the same biopsies were assayed to determine the effect of cell position within the gastric pit on DNA damage. Results. DNA damage was significantly higher in normal gastric mucosa than in H. pylori gastritis [median (interquartile range) 65% (58.5,75.8), n = 18 and 21% (11.9,29.8), n = 65, respectively, p < .001]. Intermediate levels were found in reactive gastritis [55.5% (41.3,71.7), n = 13] and H. pylori negative chronic gastritis [50.5% (36.3,60.0), n = 15]. DNA damage rose 6 weeks after successful eradication of H. pylori[to 39.5% (26.3,51.0), p = .007] but was still lower than in normal mucosa. Chronic inflammation was the most important histological factor that determined DNA damage. DNA damage fell with increasing digestion times (r = ,.92 and ,.88 for normal mucosa and H. pylori gastritis, respectively). Conclusions. Lower levels of DNA damage in cells isolated from H. pylori infected gastric biopsies may be a reflection of increased cell turnover in H. pylori gastritis. The investigation of mature gastric epithelial cells for DNA damage is unlikely to elucidate the mechanisms underlying gastric carcinogenesis. [source] Cryopreservation of fish sperm: applications and perspectivesJOURNAL OF APPLIED ICHTHYOLOGY, Issue 5 2010E. Cabrita Summary Cryopreservation is of interest not only for fish farming but also for the conservation and genetic improvement of resources. This technique has been well established in some freshwater fish species mainly, salmonid, sturgeons and carps, however, only in the last decade research was focused in marine fish species. The benefits of sperm cryopreservation include: (i) synchronization of gamete availability of both sexes, (ii) sperm economy; (iii) simplification of broodstock management, (iv) transport of gametes from different fish farms, and (v) germplasm storage for genetic selection programs or conservation of species. These issues would certainly benefit the aquaculture industry. The tremendous impact that biotechnology is having in aquaculture has been particularly obvious in recent years. Several species are being used as research models not only for aquaculture development applications but also for medical research. Sperm cryopreservation can give an important contribution in the germ storage of all transgenic lines. However, in all applications in fish sperm, cryopreservation needs to overcome a lack in standardization of methodologies and procedures, a correct assay of seminal quality and the development of tools to characterize cryoinjury. Many efforts have recently been made in the study of DNA using different approaches such as the comet assay (single cell gel electrophoresis), TUNEL (terminal deoxynucleotidyl transferase-nick-end-labelling), SCSA (sperm chromatin structure assay) and the analysis of specific DNA sequences using RT-PCR, since DNA damage may impair fertility or embryo development. Cryopreservation of gametes would certainly benefit from a higher concern on male improvement, basically through nutrition or selection of resistant stocks (e.g. stress resistant individuals or highly adapted to captivity) producing gametes of higher quality. There is a huge window of opportunities for improve the resistance of cells to cryopreservation through diet supplementation of certain compounds such as amino acids (taurine and hypotaurine), vitamins (Vit. E and C) and lipids or through a direct supplementation of the extender media. An equilibrium of those compounds will improve spermatozoa and seminal plasma composition protecting cells against oxidative stress (lipid peroxidation, protein oxidation, DNA fragmentation, enzyme protection) that is gaining each day more importance in cryodamage research. [source] Naringin, a grapefruit flavanone, protects V79 cells against the bleomycin-induced genotoxicity and decline in survivalJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2007Abhinav Jagetia Abstract The effect of naringin, a grapefruit flavonone was studied on bleomycin-induced genomic damage and alteration in the survival of cultured V79 cells. Exposure of V79 cells to bleomycin induced a concentration dependent elevation in the frequency of binucleate cells bearing micronuclei (MNBNC) and a maximum number of MNBNCs were observed in the cells treated with 50 ,g ml,1 bleomycin, the highest concentration evaluated. This genotoxic effect of bleomycin was reflected in the cell survival, where a concentration dependent decline was observed in the cells treated with different concentrations of bleomycin. Treatment of cells with 1 mm naringin before exposure to different concentrations of bleomycin arrested the bleomycin-induced decline in the cell survival accompanied by a significant reduction in the frequency of micronuclei when compared with bleomycin treatment alone. The cell survival and micronuclei induction were found to be inversely correlated. The repair kinetics of DNA damage induced by bleomycin was evaluated by exposing the cells to 10 ,g ml,1 bleomycin using single cell gel electrophoresis. Treatment of V79 cells with bleomycin resulted in a continuous increase in DNA damage up to 6 h post-bleomycin treatment as evident by migration of more DNA into the tails (% tail DNA) of the comets and a subsequent increase in olive tail moment (OTM), an index of DNA damage. Treatment of V79 cells with 1 mm naringin reduced bleomycin-induced DNA damage and accelerated DNA repair as indicated by a reduction in % tail DNA and OTM with increasing assessment time. A maximum reduction in the DNA damage was observed at 6 h post-bleomycin treatment, where it was 5 times lower than bleomycin alone. Our study, which was conducted on the basis of antioxidant, free radical scavenging and metal chelating properties of naringin demonstrates that naringin reduced the genotoxic effects of bleomycin and consequently increased the cell survival and therefore may act as a chemoprotective agent in clinical situations. Copyright © 2006 John Wiley & Sons, Ltd. [source] Inhibitory effect of magnolol on Trp-P-2-induced DNA damage in various organs in micePHYTOTHERAPY RESEARCH, Issue 7 2009Junichiro Saito Abstract Magnolol has been reported to strongly inhibit the mutagenicity induced by indirect mutagens in the Ames test as well as the clastogenicity induced by benzo(a)pyrene (B(a)P) in the mice micronucleus test. Here, we evaluated the inhibitory effect of magnolol on the DNA damage induced by 3-amino-1-methyl-5H -pyrido[4,3-b]indole (Trp-P-2) in various organs using the mice alkaline single cell gel electrophoresis (SCG) assay. Animals were treated with a single oral administration of magnolol (0.01, 0.1, 1, 10, and 100 mg/kg), followed by a single intraperitoneal injection of Trp-P-2 (10 mg/kg). The liver, lung, and kidney were removed at 3 h after treatment and used in SCG assay. The results indicated that magnolol inhibited Trp-P-2-induced DNA damage in various organs. To elucidate the mechanism of this inhibitory effect against Trp-P-2, we investigated the inhibitory effect of magnolol on in vivo CYP1A2 activity using the zoxazolamine paralysis test. Magnolol significantly prolonged zoxazolamine paralysis time and showed an inhibitory effect on in vivo CYP1A2 activity. These results indicate that magnolol has an inhibitory effect on the DNA damage induced by Trp-P-2 in various organs in vivo. This inhibitory mechanism is considered due to in vivo CYP1A2 inhibition. Copyright © 2009 John Wiley & Sons, Ltd. [source] Preventive Effects of Quercetin against Benzo[a]pyrene-Induced DNA Damages and Pulmonary Precancerous Pathologic Changes in MiceBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2006Nian-zu Jin In this study, mice in quercetin-treated groups were given quercetin for 90 days. After one week of treatment, mice in the quercetin-treated groups and the positive control group received a single intraperitoneal dose of benzo[a]pyrene (100 mg/kg body weight). The results of single cell gel electrophoresis assay showed that the average lengths of the comet cell tail and DNA damage in the peripheral blood lymphocytes of mice induced by benzo[a]pyrene decreased significantly as a result of quercetin treatment dose-dependently. Light microscopic examination showed that the degrees of pulmonary precancerous pathologic changes in the quercetin-treated groups decreased significantly compared with those in the positive control group. Meanwhile, the cytochrome P4501A1-linked 7-ethoxyresorufin O-dealkylase activities in lung microsomes of mice decreased as the dose of quercetin increased. The results of this in vivo study revealed that quercetin had a significant preventive effect on benzo[a]pyrene-induced DNA damage, and had a potential chemopreventive effect on the carcinogenesis of lung cancer induced by benzo[a]pyrene. The mechanism of these effects of quercetin could be related to the inhibition of cytochrome P4501A1 activity. [source] A novel, rapid, inexpensive, and highly sensitive experiment for demonstration of DNA damage in human leukocytes by single cell gel electrophoresisBIOCHEMISTRY AND MOLECULAR BIOLOGY EDUCATION, Issue 1 2003B. R. Manjunatha Abstract The single cell gel electrophoresis technique (comet assay) has been adopted to demonstrate the DNA damage in human leukocytes of individuals who are habitual smokers. This technique allows the detection of single strand and double strand DNA breaks, which are indicative of the risk of cancer. The method followed is rapid, inexpensive, and a highly sensitive technique for the evaluation of DNA damage and risk assessment in smokers. This experiment should help students understand the effect of cigarette smoking. [source] Evaluation of genotoxic effects in human leukocytes after in vitro exposure to 1950 MHz UMTS radiofrequency fieldBIOELECTROMAGNETICS, Issue 3 2008O. Zeni Abstract In the present study the third generation wireless technology of the Universal Mobile Telecommunication System (UMTS) signal was investigated for the induction of genotoxic effects in human leukocytes. Peripheral blood from six healthy donors was used and, for each donor, intermittent exposures (6 min RF on, 2 h RF off) at the frequency of 1950 MHz were conducted at a specific absorption rate of 2.2 W/kg. The exposures were performed in a transverse electro magnetic (TEM) cell hosted in an incubator under strictly controlled conditions of temperature and dosimetry. Following long duration intermittent RF exposures (from 24 to 68 h) in different stages of the cell cycle, micronucleus formation was evaluated by applying the cytokinesis block micronucleus assay, which also provides information on cell division kinetics. Primary DNA damage (strand breaks/alkali labile sites) was also investigated following 24 h of intermittent RF exposures, by applying the alkaline single cell gel electrophoresis (SCG)/comet assay. Positive controls were included by treating cell cultures with Mitomycin-C and methylmethanesulfonate for micronucleus and comet assays, respectively. The results obtained indicate that intermittent exposures of human lymphocytes in different stages of cell cycle do not induce either an increase in micronucleated cells, or change in cell cycle kinetics; moreover, 24 h intermittent exposures also fail to affect DNA structure of human leukocytes soon after the exposures, likely indicating that repairable DNA damage was not induced. Bioelectromagnetics 29:177,184, 2008. © 2007 Wiley-Liss, Inc. [source] Evaluation of genotoxic effects in human peripheral blood leukocytes following an acute in vitro exposure to 900 MHz radiofrequency fieldsBIOELECTROMAGNETICS, Issue 4 2005O. Zeni Abstract 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 °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. Bioelectromagnetics 26:258,265, 2005. © 2005 Wiley-Liss, Inc. [source] Genotoxicity of radiofrequency signals.BIOELECTROMAGNETICS, Issue 2 2002Abstract As part of a comprehensive investigation of the potential genotoxicity of radiofrequency (RF) signals emitted by cellular telephones, in vitro studies evaluated the induction of DNA and chromosomal damage in human blood leukocytes and lymphocytes, respectively. The signals were voice modulated 837 MHz produced by an analog signal generator or by a time division multiple access (TDMA) cellular telephone, 837 MHz generated by a code division multiple access (CDMA) cellular telephone (not voice modulated), and voice modulated 1909.8 MHz generated by a global system of mobile communication (GSM)-type personal communication systems (PCS) cellular telephone. DNA damage (strand breaks/alkali labile sites) was assessed in leukocytes using the alkaline (pH>13) single cell gel electrophoresis (SCG) assay. Chromosomal damage was evaluated in lymphocytes mitogenically stimulated to divide postexposure using the cytochalasin B-binucleate cell micronucleus assay. Cells were exposed at 37±1°C, for 3 or 24 h at average specific absorption rates (SARs) of 1.0,10.0 W/kg. Exposure for either 3 or 24 h did not induce a significant increase in DNA damage in leukocytes, nor did exposure for 3 h induce a significant increase in micronucleated cells among lymphocytes. However, exposure to each of the four RF signal technologies for 24 h at an average SAR of 5.0 or 10.0 W/kg resulted in a significant and reproducible increase in the frequency of micronucleated lymphocytes. The magnitude of the response (approximately four fold) was independent of the technology, the presence or absence of voice modulation, and the frequency (837 vs. 1909.8 MHz). This research demonstrates that, under extended exposure conditions, RF signals at an average SAR of at least 5.0 W/kg are capable of inducing chromosomal damage in human lymphocytes. Bioelectromagnetics 23:113,126, 2002. © 2002 Wiley-Liss, Inc. [source] | |||||||||||||