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Comet
Kinds of Comet Terms modified by Comet Selected AbstractsEvaluation 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] No increases in biomarkers of genetic damage or pathological changes in heart and brain tissues in male rats administered methylphenidate hydrochloride (Ritalin) for 28 days,,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2010Kristine L. Witt Abstract Following a 2005 report of chromosomal damage in children with attention deficit/hyperactivity disorder (ADHD) who were treated with the commonly prescribed medication methylphenidate (MPH), numerous studies have been conducted to clarify the risk for MPH-induced genetic damage. Although most of these studies reported no changes in genetic damage endpoints associated with exposure to MPH, one recent study (Andreazza et al. [2007]: Prog Neuropsychopharmacol Biol Psychiatry 31:1282,1288) reported an increase in DNA damage detected by the Comet assay in blood and brain cells of Wistar rats treated by intraperitoneal injection with 1, 2, or 10 mg/kg MPH; no increases in micronucleated lymphocyte frequencies were observed in these rats. To clarify these findings, we treated adult male Wistar Han rats with 0, 2, 10, or 25 mg/kg MPH by gavage once daily for 28 consecutive days and measured micronucleated reticulocyte (MN-RET) frequencies in blood, and DNA damage in blood, brain, and liver cells 4 hr after final dosing. Flow cytometric evaluation of blood revealed no significant increases in MN-RET. Comet assay evaluations of blood leukocytes and cells of the liver, as well as of the striatum, hippocampus, and frontal cortex of the brain showed no increases in DNA damage in MPH-treated rats in any of the three treatment groups. Thus, the previously reported observations of DNA damage in blood and brain tissue of rats exposed to MPH for 28 days were not confirmed in this study. Additionally, no histopathological changes in brain or heart, or elevated serum biomarkers of cardiac injury were observed in these MPH-exposed rats. Environ. Mol. Mutagen. 2010. Published 2009 Wiley-Liss, Inc. [source] Arsenate and dimethylarsinic acid in drinking water did not affect DNA damage repair in urinary bladder transitional cells or micronuclei in bone marrow,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 9 2009Amy Wang Abstract Arsenic is a human skin, lung, and urinary bladder carcinogen, and may act as a cocarcinogen in the skin and urinary bladder. Possible modes of action of arsenic carcinogenesis/cocarcinogenesis include oxidative stress induction and inhibition of DNA damage repair. We investigated the effects of arsenic in drinking water on DNA damage repair in urinary bladder transitional cells and on micronucleus formation in bone marrow. F344 rats were given 100 ppm arsenate [As(V)] or dimethylarsinic acid [DMA(V)] in drinking water for 1 week. The in vivo repair of cyclophosphamide (CP)-induced DNA damage resulting from a single oral gavage of CP, and the in vitro repair of hydrogen peroxide (H2O2)- or formaldehyde-induced DNA damage, resulting from adding H2O2 or formaldehyde into cell medium, were measured by the Comet assay. DMA(V) effects were not observed on either CP-induced DNA damage induction or on DNA repair. Neither DMA(V) nor As(V) increased the H2O2 - or formaldehyde-induced DNA damage, and neither inhibited the repair of H2O2 -induced DNA damage. Neither DMA(V) nor As(V) increased the micronucleus frequency, nor did they elevate micronucleus frequency resulting from CP treatment above the level observed by the treatment with CP alone. These results suggest that arsenic carcinogenesis/cocarcinogenesis in the urinary bladder may not be via DNA damage repair inhibition. To our knowledge this is the first report of arsenic effects on DNA damage repair in the urinary bladder. Environ. Mol. Mutagen. 2009. Published 2009 by Wiley-Liss, Inc. [source] Improved Comet assay for the assessment of UV genotoxicity in Mediterranean sea urchin eggsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2008Sarah Nahon Abstract Gametes and embryos of broadcast spawners are exposed to a wide range of chemical and physical stressors which may alone, or in conjunction, have serious consequences on reproductive outcomes. In this study, two Mediterranean echinoid species, Paracentrotus lividus and Sphaerechinus granularis, were chosen as models to study the genotoxicity of UV radiation (UVR) on the eggs of broadcast-spawning marine invertebrates. The single cell gel electrophoresis, or Comet assay, was successfully adapted to assess DNA strand breakage in sea urchin eggs. The results demonstrated that the genetic material of sea urchin eggs is susceptible to environmentally realistic UV exposure. The induction of DNA damage in the irradiated unfertilized eggs suggests that the previously described defense mechanisms in sea urchin eggs do not completely protect the egg's DNA against UV toxicity. Taken together, our results suggest that UV-impairment of the genetic integrity of the eggs might have a role in postfertilization failures and abnormal embryonic development. Although both species were vulnerable to UVR, embryonic development was less dramatically impaired in P.Lividus. This observation supports the postulation that species inhabiting shallower environments possess more efficient mechanisms to overcome UV-induced DNA alterations. The present demonstration of the utility and sensitivity of the Comet assay to evaluate DNA integrity in eggs from marine invertebrates opens new perspectives for monitoring the long-term effects of environmental exposure on populations and for the routine screening of substances for genotoxicity in marine systems. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. [source] DNA damage and repair capacity in lymphocytes from obstructive sleep apnea patientsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 9 2007Konstantina Kontogianni Abstract Obstructive sleep apnea (OSA) syndrome is a respiratory disease that is linked to heart attacks and high blood pressure. In the present study, we used the Comet assay to compare basal DNA damage and DNA damage induction by hydrogen peroxide, ethanol, and ,-irradiation in lymphocytes from 35 OSA patients and 35 controls. We also measured the apoptosis and necrosis produced by these agents and the ability of the lymphocytes to repair the induced DNA damage. It was found that lymphocytes isolated from OSA patients had higher basal levels of DNA damage and were more sensitive to the effects of the DNA-damaging agents than lymphocytes from controls. OSA patients also had a reduced capacity to repair the DNA damage induced by the three agents, but apoptosis and necrosis were similar in OSA patients and the controls. Environ. Mol. Mutagen., 2007. © 2007 Wiley-Liss, Inc. [source] Lack of genotoxicity induced by endogenous and synthetic female sex hormones in peripheral blood cells detected by alkaline comet assayENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2007Mariana Gobbo Braz Abstract The etiology of hormone-induced cancers has been considered to be a combination of genotoxic and epigenetic events. Currently, the Comet assay is widely used for detecting genotoxicity because it is relatively simple, sensitive, and capable of detecting various kinds of DNA damage. The present study evaluates the genotoxic potential of endogenous and synthetic sex hormones, as detected by the Comet assay. Blood cells were obtained from 12 nonsmoking and 12 smoking women with regular menstrual cycles and from 12 nonsmoking women taking low-dose oral contraceptives (OC). Peripheral blood samples were collected at three phases of the menstrual cycle (early follicular, mean follicular, and luteal phases), or at three different moments of oral contraceptive intake. Three blood samples were also collected from 12 healthy nonsmoking men, at the same time as oral contraceptive users. Results showed no significant difference in the level of DNA damage among the three moments of the menstrual cycle either in nonsmoking and smoking women, or between them. No significant difference in DNA damage was also observed among oral contraceptive users, nonusers, and men. Together, these data indicate lack of genotoxicity induced by the physiological level of the female sex hormones and OC as assessed by the alkaline Comet assay. In conclusion, normal fluctuation in endogenous sex hormones and use of low-doses of oral contraceptive should not interfere with Comet assay data when this technique is used for human biomonitoring. Environ. Mol. Mutagen., 2007. © 2007 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] DNA damage and repair measurements from cryopreserved lymphocytes without cell culture,A reproducible assay for intervention studiesENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 7 2006Jyh-Lurn Chang Abstract Single-cell gel electrophoresis (the Comet assay) can be used to measure DNA damage and DNA repair capacity (DRC). However, to test DRC of cryopreserved lymphocytes, published methods include steps for cell culturing and phytohemagglutinin stimulation, which may limit use of this assay in intervention studies. We developed a modified Comet assay protocol that allows us to measure DRC from cryopreserved lymphocytes without these in vitro manipulations. Assay reproducibility was evaluated by performing the assay six times on different dates using six aliquots from one blood draw of one individual. The interindividual variation was assessed by performing the assay using one aliquot from six individuals. When ,-irradiation was used as the mutagen, intra-assay coefficients of variation (CVs.) for baseline DNA damage, damage after ,-irradiation exposure, and DRC,measured as tail moment,were 8, 31, and 10%, respectively. Interindividual CVs. were higher. When H2O2 was used as the mutagen, intra-assay CVs. for damage measurements were lower for a protocol modification that included damage and repair at 37°C (CVs. ranging from 8 to 35%) than for the more standard 4°C protocol. Analyzing moment arm,the average distance of DNA migration within the tail,yielded similar results. DNA repair was successfully detected in each experiment. Comparing freshly isolated lymphocytes to cryopreserved lymphocytes from the same individuals' blood draw indicated that DRC was highly correlated when determined using moment arm values. This modified protocol extends the use of the Comet assay to measuring DRC in intervention studies (e.g., dietary interventions) in that it assesses cellular response after cryopreservation without cell culture or other extensive manipulation. Environ. Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source] In vivo genotoxic effects of industrial waste leachates in mice following oral exposureENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2006Saurabh Chandra Abstract Contamination of ground water by industrial waste poses potential health hazards for man and his environment. The improper disposal of toxic wastes could allow genotoxic chemicals to percolate into ground waters, and these contaminated ground waters may produce toxicity, including mutation and eventually cancer, in exposed individuals. In the present study, we evaluated the in vivo genotoxic potential of leachates made from three different kinds of industrial waste (tannery waste, metal-based waste, and waste containing dyes and pigments) that are disposed of in areas adjoining human habitation. Three different doses of test leachates were administered by oral gavage for 15 consecutive days to Swiss albino mice; their bone marrow cells were examined for chromosome aberrations (CAs), micronucleated polychromatic erythrocytes (MNPCEs), and DNA damage using the alkaline Comet assay. Exposure to the leachates resulted in significant (P < 0.05 or P < 0.001) dose-dependent increases in chromosome and DNA damage. Fragmented chromosomes and chromatid breaks were the major CAs observed. Chemical analysis of the leachates indicated that chromium and nickel were elevated above the limits established by health organizations. The highest levels of genotoxicity were produced by the metal-based leachate and the tannery-waste leachate, while the dye-waste leachate produced weaker genotoxic responses. The cytogenetic abnormalities and DNA damage produced by the leachates indicate that humans consuming water contaminated with these materials are at increased risk of developing adverse health consequences. Environ. Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source] DNA damage in mice treated with sulfur dioxide by inhalationENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2005Ziqiang Meng Abstract Sulfur dioxide (SO2) is a ubiquitous air pollutant produced by the burning of fossil fuels. In this study, single-cell gel electrophoresis (the Comet assay) was used to evaluate the DNA damage produced by inhalation exposure of mice to SO2. Male and female mice were housed in exposure chambers and treated with 14.00 ± 1.25, 28.00 ± 1.98, 56.00 ± 3.11, and 112.00 ± 3.69 mg/m3 SO2 for 6 hr/day for 7 days, while control groups were exposed to filtered air. Comet assays were performed on blood lymphocytes and cells from the brain, lung, liver, spleen, kidney, intestine, and testicles of the animals. SO2 caused significant, dose-dependent increases in DNA damage, as measured by Olive tail moment, in all the cell types analyzed from both sexes of mice. The results indicate that inhalation exposure to SO2 damages the DNA of multiple organs in addition to the lung, and suggests that this damage could result in mutation, cancer, and other diseases related to DNA damage. Further work will be required to understand the ultimate toxicological significance of this damage. These data also suggest that detecting DNA damage in blood lymphocytes, using the Comet assay, may serve as a useful tool for evaluating the impact of pulmonary SO2 exposure in human biomonitoring studies. Environ. Mol. Mutagen., 2005. © 2005 Wiley-Liss, Inc. [source] DNA damage in leukocytes of workers occupationally exposed to arsenic in copper smeltersENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2005Jadwiga Palus Abstract Inorganic arsenic (i-As) is a known human carcinogen; however, humans continue to be exposed to i-As in drinking water and in certain occupational settings. In this study, we used the Comet assay to evaluate DNA damage in the somatic cells of workers from three Polish copper smelters who were occupationally exposed to i-As. Blood samples were collected from 72 male workers and 83 unexposed male controls and used for the detection of DNA damage, oxidative DNA damage, and DNA damage after a 3-hr incubation in culture. Urine samples were collected to assess the level of exposure. The mean concentration of arsenic metabolites in urine [the sum of arsenite (AsIII), arsenate (AsV), monomethylarsenate (MMA) and dimethylarsenate (DMA)] and the concentrations of DMA (the main metabolite in urine) were higher in workers than in controls, but the differences were not statistically significant. By contrast, the level of DNA damage, expressed as the median tail moment, was significantly higher in the leukocytes of workers than in the controls. Comet assays conducted with formamidopyrimidine glycosylase (FPG) digestion to detect oxidative DNA damage indicated that oxidative lesions were present in leukocytes from both the exposed and control groups, but the levels of damage were significantly higher among the workers. Incubation of the cells in culture resulted in a significant reduction in the levels of DNA damage, especially among leukocytes from the workers, suggesting that the DNA damage was subject to repair. Our findings indicate that copper smelter workers have increased levels of DNA damage in somatic cells, suggesting a potential health risk for the workers. Although i-As was present in air samples from the smelters and in urine samples from workers, no clear association could be made between i-As exposure and the DNA damage. Environ. Mol. Mutagen., 2005. © 2005 Wiley-Liss, Inc. [source] Modifying effect of propolis on dimethylhydrazine-induced DNA damage but not colonic aberrant crypt foci in ratsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2005Rodrigo O. Alves de Lima Abstract Propolis is a honeybee product with several biological and therapeutic properties, including antimutagenic and anticarcinogenic activities. The effects of an aqueous extract of propolis (AEP) were evaluated on the formation of 1,2-dimethylhydrazine (DMH)-induced aberrant crypt foci (ACF) and DNA damage in the colon of male Wistar rats by the ACF and Comet assays, respectively. AEP was administered orally at 0.01%, 0.03%, 0.1%, and 0.3% in the drinking water, which resulted in doses of approximately 12, 34, 108, and 336 mg/kg body weight/day. Animals were also given a single subcutaneous injection of 40 mg/kg DMH and sacrificed 4 hr later for evaluating DNA damage, or 4 doses of 40 mg/kg DMH, administered 2 doses/week for 2 weeks, and sacrificed 12 weeks after the last injection for evaluating ACF development in the distal colon. Administration of AEP either simultaneously with or after the DMH treatment resulted in no statistically significant reduction of ACF. In contrast, 0.01%, 0.03%, and 0.3% AEP, given simultaneously with DMH, reduced DNA damage induction in the mid and distal colon. However, 0.3% AEP alone increased DNA damage in the colon. In conclusion, AEP had no effect on the formation of DMH-induced ACF in rat colon, but it modulated DMH-induced DNA damage in colon cells. Further investigations are recommended in order to establish the conditions under which propolis produces either protective or deleterious effects. Environ. Mol. Mutagen., 2005. © 2004 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] Genotoxicity related to transfer of oil spill pollutants from mussels to mammals via foodENVIRONMENTAL TOXICOLOGY, Issue 4 2004Sébastien Lemiere Abstract Heavy fuel oils containing high levels of polycyclic aromatic hydrocarbons (PAHs) were released into the marine environment after the Erika oil spill on the Atlantic coast. As highly condensed PAH pollutants can bioaccumulate in invertebrates, their transfer to vertebrates through the food chain was of concern. This study aimed to estimate potential genotoxic effects in rats fed for 2 or 4 weeks with the marine mussel Mytilus edulis contaminated by oil pollutants. Two levels of PAH contamination were studied, around 100 and 500 ,g of total PAHs/kg dry weight (d.w.) in mussels. Genotoxic damage in rats was investigated by single-cell gel electrophoresis (Comet assay) and micronucleus assays in liver, bone marrow, and peripheral blood. DNA damage was observed in the liver of rats fed with the most contaminated mussels (500 ,g PAHs/kg d.w.).DNA damage also was observed in the bone marrow but less than that in the liver. A small increase in micronuclei frequency was registered as well. This work underlines the bioavailability of pollutants in fuel-oil-contaminated mussels to consumers and the usefulness of the Comet assay as a sensitive tool in biomonitoring to analyze responses to PAH transfer in food. The occurrence of substituted PAHs and related compounds such as benzothiophenes in addition to nonsubstituted PAHs in fuel oils and mussels raised the question of whether they were implicated in the genotoxic effects registered in rats. © 2004 Wiley Periodicals, Inc. Environ Toxicol 19: 387,395, 2004. [source] The relationship between obesity and markers of oxidative stress in dogsJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 2 2009M. G. Cline Obesity, a serious epidemic affecting much of our pet population, increases the risk of developing numerous diseases. It has been demonstrated that obesity increases oxidative stress in obese children, cats and other species. Oxidative stress can result in DNA damage with subsequent alterations in gene expression, cell signaling, mutations, cell death or cell transformation. These effects of oxidative damage predispose animals and humans to numerous disease processes and cancer. The objective of the study was to demonstrate that obese dogs are under oxidative stress resulting in DNA damage and decreased endogenous antioxidant protection measured by serum glutathione levels and the ratio of reduced (GSH) to oxidized (GSSG) glutathione. In this case,control study, 10 obese dogs were compared with aged-matched healthy control dogs. Dogs with BCS of 7 or greater (9 pt scale) were considered obese. Dogs were evaluated by history, physical exam, body condition score, CBC, serum biochemical analysis and total T4, with both groups showing no significant differences in CBC, serum biochemical or T4 analysis. Single-cell gel electrophoresis (Comet assay) was used to measure DNA damage, and high performance liquid chromatography was used to measure serum glutathione. Reduced glutathione levels were significantly higher in the obese group (p = 0.012). The results of this pilot study suggest that obesity is associated with an increase in antioxidant potential, therefore justifying a larger study with antioxidant supplementation to determine how antioxidants in weight loss diets effects endogenous antioxidant capabilities. [source] Evaluation of cytogenetic effects of lambda-cyhalothrin on human lymphocytesJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2005Rambabu Naravaneni Abstract The genotoxic and cytotoxic potential of lambda-cyhalothrin (LCT), a synthetic pyrethroid insecticide, was investigated on human lymphocytes cultured in vitro. Utilizing the trypan blue dye exclusion technique assay, the LC50 of LCT was found to be 28 , M. Based on the LC50 value, it is seen that LCT was highly toxic to lymphocyte cultures, among other pyrethroid group of pesticides. Chromosomal aberrations induced by LCT were determined using metaphase plate-spreads of lymphocytes. The chromosomal analysis was recorded using Medi-Image software technology. The analysis revealed that more satellite associations and gaps were found, which were statistically significant (p < 0.05) when compared to controls. Comet assay was used to assess the possibility of LCT to induce the damage in DNA, where the increase in comet tail length relates to the extent of DNA single strand breaks. The results presented here indicate that in vitro assays could be used as indicators of cytotoxicity and genotoxicity of the pesticide. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:304,310, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20095 [source] In vitro antioxidant activities of mouthrinses and their componentsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 5 2002M. Battino Abstract Objectives: Several forms of periodontal diseases (PD) are often associated with activated phagocytosing leukocytes and contemporary free radical production. Host antioxidant defenses could benefit from mouthrinses used as adjuncts to counteract plaque-associated bacteria. The aim of the present study was to determine possible antioxidant activity (AA) of a number of antiseptic mouthrinses and of their stated active principles (AP), regardless of their efficacy as antimicrobial agents. Material and Methods: The antioxidant activities of 11 mouthrinses and their active principles were tested with a specific spectrophotometric method. Comet assay was used to test whether pure chemical antioxidant activity actually corresponded to prevention of in vitro DNA fragmentation. Results: Methylsalicylate-containing mouthrinses were the most effective. Several compounds, and some vehicles, behaved as antioxidants. Fibroblast DNA fragmentation was limited by preincubation with methylsalicylate-containing mouthrinse but was unaffected by treatment with chlorexidine. Conclusion: The results described herein indicate that several mouthrinses possess AA; such a property could be ascribed to either AP or vehicles or both. All the data were obtained in systems in vitro and the demonstration of in vivo AA is necessary. These findings could be useful in the treatment of some forms of PD and should be considered when arranging new mouthrinse formulations. Zusammenfassung In vitro antioxidative Aktivitäten von Mundwässern und ihren Komponenten Ziele:,Verschiedene Formen von parodontalen Erkrankungen (PD) sind häufig mit aktivierten phagozytierenden Leukozyten und gleichzeitiger Produktion von freien Radikalen verbunden. Die Antioxydantienabwehr des Wirtes könnte von Mundwässern genützt werden, die als Adjunktive zur Bekämpfung der plaque-assoziierten Bakterien verwendet werden. Das Ziel der vorliegenden Studie war die Bestimmung der möglichen Antioxydantienaktivität (AA) von einer Anzahl antiseptischer Mundwässer und ihrer angegebenen aktiven Prinzipien (AP), unabhängig von ihrer Effektivität als antimikrobielle Agentien. Material und Methoden:,Die antioxydative Aktivität von 11 Mundwässern und ihre Aktivitätsprinzipien wurden mit einer spezifischen Spektralphotometrie getestet. Ein Assay wurde für die Testung genutzt, ob die reine chemische antioxydative Aktivität tatsächlich mit der Prävention der in vitro DNA Fragmentation korrespondiert. Ergebnisse:,Methylsalicylat enthaltende Mundwässer waren am effektivsten. Verschiedene Bestandteile und einige Vehikel verhielten sich wie Antioxydantien. Fibroblasten DNA Fragmentation wurde durch Präinkubation mit Methylsalicylat enthaltende Mundwässer begrenzt, war aber unbeeinflusst durch Behandlung mit Chlorhexidin. Schlussfolgerung:,Die beschriebenen Ergebnisse zeigen, dass verschiedene Mundwässer über AA verfügen; solch eine Eigenschaft könnte entweder AP oder Vehikeln oder beiden zugeschrieben werden. Alle Daten sind in in vitro Systemen gewonnen worden, aber die Demonstration der in vivo AA ist notwendig. Diese Ergebnisse könnten in der Behandlung von einigen Formen der PD nützlich sein und sollten bei der Entwicklung neuer Mundwasserrezepte beachtet werden. Résumé Activité antioxydante in vitro des bains de bouche et de leurs composants Buts:,Plusieurs formes d'affections parodontales (periodontal diseases, PD) sont souvent associées à des leucocytes phagocytaires activés et à la production de radicaux libres contemporains. L'utilisation de bains de bouche comme adjuvants pourrait être bénéfique aux défenses antioxidantes de l'hôte pour lutter contre les bactéries de plaque. L'objectif de cette étude était de déterminer l'activité antioxydante (antioxidant activity, AA) potentielle d'un certain nombre de bains de bouche antiseptiques et de leurs principes actifs reconnus (active principles, AP), indifféremment de leur efficacité en tant qu'agents antimicrobiens. Matériaux et méthodes:,L'activité antioxydante de 11 bains de bouche et de leurs principes actifs a été testée à l'aide d'une méthode spectrophotométrique spécifique. Le test Comet a été utilisé pour voir si l'activité antioxydante chimique pure permet effectivement de prévenir la fragmentation de l'ADN in vitro. Résultats:,Les bains de bouche contenant du méthylsalicylate étaient les plus efficaces. Plusieurs composés et certains vecteurs se comportaient comme des antioxydants. La pré-incubation dans des bains de bouche contenant du méthylsalicylate limitait la fragmentation de l'ADN des fibroblastes, mais le traitement à la chlorhexidine ne l'affectait pas. Conclusion:,Les résultats décrits dans cette étude indiquent que plusieurs bains de bouche possèdent une AA, propriété qui pourrait être attribuée aux AP ou aux véhicules ou aux deux. Toutes les données ont été obtenues sur des systèmes in vitro, et l'AA in vivo reste à démontrer. Ces résultats pourraient s'avérer utiles pour le traitement de certaines formes de PD et devraient être pris en compte lors de l'élaboration de nouvelles formulations de bains de bouche. [source] Identification of Irradiated Spices Using the Novel Technique of DNA Comet AssayJOURNAL OF FOOD SCIENCE, Issue 2 2002A.A. Khan ABSTRACT: Microgel electrophoresis of single cells or nuclei (DNA comet assay) was investigated to identify irradiated spices. Ten spices treated with radiation doses in the range of 0 to 20 kGy were analyzed. After electrophoresis, radiation-damaged DNA appeared as a comet, whereas in non irradiated spices round or conical spots appeared. Shape, length, and intensity of comets were also dose-dependent. Detection was successful in poppy seeds, cardamom seeds, caraway seeds, and nigella seeds, but not in pomegranate seeds, ginger root, and juniper berries, where lysis was insufficient, and also not in black peppercorns, nutmeg seed, and rosemary leaves, where extraction of cells or nuclei failed. Nevertheless, for some irradiated foods the DNA comet assay is a rapid and inexpensive screening test. [source] Novel quinolone CHM-1 induces apoptosis and inhibits metastasis in a human osterogenic sarcoma cell lineJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 12 2009Shu-Chun Hsu Abstract Novel 2-phenyl-4-quinolone compounds have potent cytotoxic effects on different human cancer cell lines. In this study, we examined anticancer activity and mechanisms of 20-fluoro-6,7-methylenedioxy-2-phenyl-4-quinolone (CHM-1) in human osterogenic sarcoma U-2 OS cells. CHM-1-induced apoptosis was determined by flow cytometric analysis, DAPI staining, Comet assay, and caspase inhibitors. CHM-1-inhibited cell migration and invasion was assessed by a wound healing assay, gelatin zymography, and a Transwell assay. The mechanisms of CHM-1 effects on apoptosis and metastasis signaling pathways were studied using Western blotting and gene expression. CHM-1 induced G2/M arrest and apoptosis at an IC50 (3 µM) in U-2 OS cells and caspase-3, -8, and -9 were activated. Caspase inhibitors increased cell viability after exposure to CHM-1. CHM-1-induced apoptosis was associated with enhanced ROS generation, DNA damage, decreased ,,m levels, and promotion of mitochondrial cytochrome c release. CHM-1 stimulated mRNA expression of caspase-3, -8, and -9, AIF, and Endo G. In addition, CHM-1 inhibited cell metastasis at a low concentration (<3 µM). CHM-1 inhibited the cell metastasis through the inhibition of MMP-2, -7, and -9. CHM-1 also decreased the levels of MAPK signaling pathways before leading to the inhibition of MMPs. In summary, CHM-1 is a potent inducer of apoptosis, which plays a role in the anticancer activity of CHM-1. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:1637,1644, 2009 [source] Modulation of oxidative cell damage by reconstituted mixtures of phenolic apple juice extracts in human colon cell linesMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 4-5 2006Sandra Schaefer Abstract Diets rich in fruits and vegetables are associated with a lower risk of tumour induction in the intestine and other sites. Apple juice with high amounts of antioxidative phenolics might protect the intestine against reactive oxygen species-mediated cell damage. We investigated to which extent the preventive effectiveness of polyphenolic juice extracts is governed by the amounts of five major constituents (rutin, phloridzin, chlorogenic acid, caffeic acid and epicatechin). In human colon cell lines (Caco-2, HT29), reconstituted mixtures of these phenolics were investigated in comparison to the original juice extracts, originating from cider and table apples. Parameters studied were (oxidative) DNA damage (Comet assay), cellular redox status (dichlorofluorescein assay) and Trolox equivalent antioxidant capacity (TEAC). The TEAC of the reconstituted mixtures was higher compared to the respective original extracts (4.7,7.3 mM vs. 3.6,4.2 mM Trolox). After 24 h cell incubation, menadione-induced (oxidative) DNA damage was more effectively reduced by the reconstituted mixtures (1,100 ,g/mL, 24 h), as compared to the original extracts. In contrast, the cellular ROS level was reduced to a rather similar extent by original extracts and reconstituted mixtures. The results lead to the conclusion that the selected constituents in their authentic proportions substantially account for the antioxidative effectiveness of phenolic apple juice extracts. [source] A combination of soy isoflavone supplementation and exercise improves lipid profiles and protects antioxidant defense-systems against exercise-induced oxidative stress in ovariectomized ratsBIOFACTORS, Issue 4 2007Hea Young Oh Abstract Menopause is often accompanied with weight gain, metabolic lipid abnormalities, and oxidative stress. In this study, we investigated the combined effects of exercise and soy isoflavone supplemention on the lipid profiles and antioxidant capacities of ovariectomized rats. Twenty-five female Sprague-Dawley rats were divided into 5 groups: sham-operated, ovariectomized (OVX), OVX with exercise (OVX + EX), OVX with soy isoflavone supplementation (OVX + ISO), and OVX with both soy isoflavones and exercise (OVX + ISO + EX). After 12 weeks of intervention, antioxidant status was evaluated in collected blood samples by the ferric reducing ability of plasma (FRAP), glutathione (GSH) content, and sodium oxide dismutase (SOD) activity. DNA damage in the lymphocytes was determined using alkaline single-cell gel electrophoresis (the Comet assay). Although there were no significant differences in weight gain and food intake, weight gain was lower in OVX + EX, OVX + ISO, and OVX + ISO + EX than in OVX. OVX + EX, OVX + ISO, and OVX + ISO + EX showed a significant decrease in total cholesterol, triglycerides, and LDL-cholesterol compared to OVX. The soy isoflavone supplemented group had significantly increased FRAP values and GSH contents in contrast to no changes in the exercised group, whereas exercise markedly increased SOD activity and H2O2 -induced DNA tail length and tail moment. Exercise with soy isoflavone supplementation significantly increased FRAP values and had no difference on SOD activity, including DNA damage. These results demonstrate that a combined treatment of moderate exercise and soy isoflavone supplementation could exert a beneficial effect on weight control and lipid profiles, and offer protection from exercise-induced oxidative stress in postmenopausal women. [source] The distant activity of Short Period Comets,, II.MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Issue 1 2008E. Mazzotta Epifani ABSTRACT The activity of the Short Period Comets (SPCs) at large heliocentric distance (Rh > 3 au) occurs in a region of the Solar system where the water sublimation rate is low and so the sublimation of other volatiles, for example CO or CO2, could drive the presence of a coma. The detection of distant activity in a SPC can therefore give important hints on its composition. Moreover, a complete characterization of the distant SPCs degree of activity is crucial in order to give correct estimates of the nucleus size and to obtain more reliable size-distribution curves of cometary nuclei. The aim of this paper is to present the last results of a program of CCD imaging of distant SPCs, started in 2004 December and concluded with observing runs at the 3.5-m Telescopio Nazionale Galileo at La Palma, in 2005 April, and at the 2.2-m Centro Astronómico Hispano Alemán (CAHA) telescope in Spain, in 2005 May. During the Spring 2005 campaign, 12 SPCs have been targeted in the R band (eight numbered SPCs and four still unnumbered SPCs): 61P/Schajn,Schaldach, 71P/Clark, 98P/Takamizawa, 103P/Hartley 2, 117P/Helin,Roman,Alu 1, 118P/Shoemaker,Levy 4, 121P/Shoemaker,Holt 2, 136P/Mueller 3, P/2002 T5 (LINEAR), P/2003 S1 (NEAT), P/2003 S2 (NEAT), P/2004 DO29 (Spacewatch,LINEAR). The heliocentric distance of the targets was 3.05 ,Rh, 5.30 au. Several levels of activity were detected in the sample, from stellar appearance to well-developed coma and tail. In some cases, the occurrence of cometary activity could be enhanced only with deep visible imaging (e.g. with very long exposure time). For comets with stellar appearance, it was possible to derive a value or a range for the nucleus radius rnucleus (assuming a ,classical' albedo value of 0.04): 98P (rnucleus= 0.43 ± 0.10 km), 136P (rnucleus= 1.2 ± 0.2 km), P/2003 S2 (rnucleus= 0.81 to 1.55 km). For the active comets, we measured dust production levels in terms of Af, quantity, which was 9.9 , Af,, 671 cm. Ensemble properties of the whole sample of the long-term program (a total of 17 SPCs) have been analysed in terms of the relationship among distant activity and dynamical evolution of the targets (in particular, an inward ,jump' of the perihelion distance): we can conclude that, even if there is some theoretical indication that this could occur, the hypothesis of distant activity triggered by a rise in perihelion temperature cannot be univocally invoked for these comets. [source] Photometry of cometary nuclei: rotation rates, colours and a comparison with Kuiper Belt Objects,MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Issue 4 2006C. Snodgrass ABSTRACT We present time-series data on Jupiter Family Comets (JFCs) 17P/Holmes, 47P/Ashbrook-Jackson and 137P/Shoemaker-Levy 2. In addition we also present results from ,snap-shot' observations of comets 43P/Wolf-Harrington, 44P/Reinmuth 2, 103P/Hartley 2 and 104P/Kowal 2 taken during the same run. The comets were at heliocentric distances of between 3 and 7 au at this time. We present measurements of size and activity levels for the snap-shot targets. The time-series data allow us to constrain rotation periods and shapes, and thus bulk densities. We also measure colour indices (V,R) and (R,I) and reliable radii for these comets. We compare all of our findings to date with similar results for other comets and Kuiper Belt Objects (KBOs). We find that the rotational properties of nuclei and KBOs are very similar, that there is evidence for a cut-off in bulk densities at ,0.6 g cm,3 in both populations, and the colours of the two populations show similar correlations. For JFCs, there is no observational evidence for the optical colours being dependent on either position in the orbit or orbital parameters. [source] Quenched large deviations for random walk in a random environmentCOMMUNICATIONS ON PURE & APPLIED MATHEMATICS, Issue 8 2009Atilla Yilmaz We take the point of view of a particle performing random walk with bounded jumps on ,d in a stationary and ergodic random environment. We prove the quenched large-deviation principle (LDP) for the pair empirical measure of the so-called environment Markov chain. By an appropriate contraction, we deduce the quenched LDP for the mean velocity of the particle and obtain a variational formula for the corresponding rate function. We propose an ansatz for the minimizer of this formula. When d = 1, we verify this ansatz and generalize the nearest-neighbor result of Comets, Gantert, and Zeitouni to walks with bounded jumps. © 2009 Wiley Periodicals, Inc. [source] Influence of DNA repair gene polymorphisms on the initial repair of MMS-induced DNA damage in human lymphocytes as measured by the alkaline comet assayENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 9 2008Charlotta Ryk Abstract We have applied the alkaline comet assay to study the functional impact of gene polymorphisms in base excision repair (APEX1 Asp148Glu, XRCC1 Arg194Trp, XRCC1 Arg399Gln) and homologous recombination repair (XRCC3 Thr241Met, NBS1 Glu185Gln), two pathways that play crucial roles in the repair of DNA damage induced by methylmethane sulphonate (MMS). We also examined the effect of polymorphisms in mismatch repair (MLH1 ,93 A/G) and nucleotide excision repair (XPD Lys751Gln) as putative negative controls based on the limited roles of these pathways in MMS-induced repair. Phytohemagglutinin-stimulated peripheral lymphocytes from 52 healthy individuals were treated with MMS and allowed to repair for 0, 15, 40, or 120 min after a 6-min washing step. DNA damage was measured as a pseudo-percentage score (comparable to % tail DNA) converted from a total visual score calculated from the distribution of cells with different degrees of damage (normal, mild, moderate and severe). The repair was faster at the beginning of the observation period than towards the end, and was not complete after 2 hr. Presence of the APEX1 148Asp, XRCC3 241Met or NBS1 185Gln alleles were significantly associated with a high pseudo-percentage score (above median) at early time points, with the APEX1 effect being most prolonged (up to 40 min after washing, odds ratio 5.6, 95% confidence interval 2.0,15.5). No significant effects were seen with the XRCC1 Arg194Trp, XRCC1 Arg399Gln, MLH1 ,93A/G and XPD Lys751Gln polymorphisms. Our results provide evidence for the functional nature of the variant alleles studied in the APEX1, XRCC3, and NBS1 genes. Environ. Mol. Mutagen., 2008. © 2008 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] Enhanced sensitivity to DNA damage induced by cooking oil fumes in human OGG1 deficient cellsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 4 2008Mei Wu Abstract Cooking oil fumes (COFs) have been implicated as an important nonsmoking risk factor of lung cancer in Chinese women. However, the molecular mechanism of COFs-induced carcinogenicity remains unknown. To understand the molecular basis underlying COFs-induced cytotoxicity and genotoxicity as well as the roles of hOGG1 in the repair of COFs-induced DNA damage, a human lung cancer cell line with hOGG1 deficiency, A549-R was established by using a ribozyme gene targeting technique that specifically knockdowned hOGG1 in A549 lung adenocarcinoma cells. MTT and comet assays were employed to examine cell viability and DNA damage/repair, respectively, in A549-R and A549 cell lines treated with COF condensate (COFC). RT-PCR and Western blot results showed that the expression of hOGG1 in A549-R cell line was significantly decreased compared with that in A549 cell line. The concentration of COFC that inhibited cell growth by 50% (the IC50) in the A549-R cell line was much lower than that in the A549 cell line, and more COFC-induced DNA damage was detected in the A549-R cell line. The time course study of DNA repair demonstrated delayed repair kinetics in the A549-R cell line, suggesting a decreased cellular damage repair capacity. Our results showed that hOGG1 deficiency enhanced cellular sensitivity to DNA damage caused by COFC. The results further indicate that hOGG1 plays an important role in repairing COF-induced DNA damage. Our study suggests that COFs may lead to DNA damage that is subjected to hOGG1 -mediated repair pathways, and oxidative DNA damage may be involved in COF-induced carcinogenesis. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. [source] Assessment of genotoxicity in rats treated with the antidiabetic agent, pioglitazoneENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2008Abdulkerim Bedir Abstract Pioglitazone (PIO), a member of the thiazolidinedione class of antidiabetic agents, specifically targets insulin resistance. Drugs of this class act as ligands for the gamma subtype of the peroxisome proliferator-activated receptor. Although troglitazone, another drug in this class, displayed unacceptable hepatotoxicity, PIO was approved for human use by the U.S. Food and Drug Administration. To our knowledge, there are no published reports on the genotoxicity of PIO; however, the package insert indicates that it has minimal genotoxicity. In this study, we used the comet assay to investigate the DNA damage in the peripheral blood and liver cells of rats treated with PIO. Sixteen male Sprague-Dawley rats were randomly distributed into four groups, and dosed daily for 14 days by oral gavage with 0, 10, 20, and 40 mg/kg/day PIO. A dose-dependent increase in DNA damage, as assessed by % tail DNA, was observed in both hepatocytes and blood lymphocytes of the PIO-treated groups, with significant increases detected between the rats treated with all the doses of PIO and the control, and between the rats treated with different PIO doses (P < 0.005 to P < 0.0001). Treating nuclei from the exposed animals with an enzyme cocktail containing Fpg and Endonuclease III prior to performing the comet assay increased the level of DNA damage, which reflects oxidized purine and pyrimidine. Taken together, our data indicate that PIO is able to dose-dependently induce DNA damage in both the liver and blood lymphocytes of rats, which is partially due to the generation of oxidative lesions. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. [source] Lack of genotoxicity induced by endogenous and synthetic female sex hormones in peripheral blood cells detected by alkaline comet assayENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2007Mariana Gobbo Braz Abstract The etiology of hormone-induced cancers has been considered to be a combination of genotoxic and epigenetic events. Currently, the Comet assay is widely used for detecting genotoxicity because it is relatively simple, sensitive, and capable of detecting various kinds of DNA damage. The present study evaluates the genotoxic potential of endogenous and synthetic sex hormones, as detected by the Comet assay. Blood cells were obtained from 12 nonsmoking and 12 smoking women with regular menstrual cycles and from 12 nonsmoking women taking low-dose oral contraceptives (OC). Peripheral blood samples were collected at three phases of the menstrual cycle (early follicular, mean follicular, and luteal phases), or at three different moments of oral contraceptive intake. Three blood samples were also collected from 12 healthy nonsmoking men, at the same time as oral contraceptive users. Results showed no significant difference in the level of DNA damage among the three moments of the menstrual cycle either in nonsmoking and smoking women, or between them. No significant difference in DNA damage was also observed among oral contraceptive users, nonusers, and men. Together, these data indicate lack of genotoxicity induced by the physiological level of the female sex hormones and OC as assessed by the alkaline Comet assay. In conclusion, normal fluctuation in endogenous sex hormones and use of low-doses of oral contraceptive should not interfere with Comet assay data when this technique is used for human biomonitoring. Environ. Mol. Mutagen., 2007. © 2007 Wiley-Liss, Inc. [source] | |||||||||||||||||||||||||