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At least 451 records · Page 25Linked to original sources
PubMed2006

Evaluation of the alkaline Comet assay conducted with the wetlands plant Bacopa monnieri L. as a model for ecogenotoxicity assessment.

Wetlands play a key role in maintaining environmental quality, and wetlands plants could serve as model organisms for determining the genotoxic effects of pollutants contaminating these areas. In the present study, DNA damage was evaluated in a wetlands plant, Bacopa monnieri L., as a potential tool for the assessment of ecogenotoxicity. The Comet assay was used for detecting DNA damage in B. monnieri exposed to two model mutagens, ethyl methanesulfonate (EMS) and methyl methanesulfonate (MMS). Significant (P < 0.05) dose-dependent increases in DNA damage were observed following treatments conducted by exposing both isolated nuclei (acellular or in vitro exposure) and whole plants (in vivo exposure) to 0.01-5 mM EMS and 0.05-100 microM MMS for 2 hr at (26 +/- 2) degrees C. The assay was then used to evaluate the genotoxic potential of cadmium (Cd), a wetlands contaminant. In vitro exposure of nuclei from untreated leaves to 0.001-200 microM Cd for 2 hr resulted in significant (P < 0.05) levels of DNA damage. Cd concentrations >or=0.01 microM induced DNA damage as evidenced by increases in the Olive tail moment. In vivo exposure of plants to 0.01-500 microM Cd for 2, 4, and 18 hr resulted in dose- and time-dependent increases in DNA damage in the nuclei isolated from roots and leaves. Cd-induced DNA damage was greater in roots than leaves. To our knowledge, this is the first report describing the use of a wetlands plant for genotoxicity assessment, using the Comet assay.

Bacopa↗
PubMed2007

In vivo exposure to microcystins induces DNA damage in the haemocytes of the zebra mussel, Dreissena polymorpha, as measured with the comet assay.

The Comet assay was used to investigate the potential of the biotoxin microcystin (MC) to induce DNA damage in the freshwater zebra mussel, Dreissena polymorpha. Mussels maintained in the laboratory were fed daily, over a 21-day period, with one of four strains of the cyanobacterium, Microcystis aeruginosa. Three of the strains produced different profiles of MC toxin, while the fourth strain did not produce MCs. The mussels were sampled at 0, 7, 14, and 21 days by withdrawing haemocytes from their adductor muscle. In addition, a positive control was performed by exposing a subsample of the mussels to water containing cadmium chloride (CdCl(2)). Cell viability, measured with the Fluorescein Diacetate/Ethidium Bromide test, indicated that the MC concentrations, to which the mussels were exposed, were not cytotoxic to the haemocytes. The Comet assay performed on the haemocytes indicated that exposure to CdCl(2) produced a dose-responsive increase in DNA damage, demonstrating that mussel haemocytes were sensitive to DNA-damaging agents. DNA damage, measured as percentage tail DNA (%tDNA), was observed in mussels exposed to the three toxic Microcystis strains, but not in mussels exposed to the nontoxic strain. Toxin analysis of the cyanobacterial cultures confirmed that the three MC-producing strains exhibit different toxin profiles, with the two MC variants detected being MC-LF and MC-LR. Furthermore, the DNA damage that was observed appeared to be strain-specific, with high doses of MC-LF being associated with a higher level of genotoxicity than low concentrations of MC-LR. High levels of MC-LF also seemed to induce relatively more persistent DNA damage than small quantities of MC-LR. This study is the first to demonstrate that in vivo exposure to MC-producing strains of cyanobacteria induces DNA damage in the haemocytes of zebra mussels and confirms the sublethal toxicity of these toxins.

Animals↗
PubMed2005

Predictors of esophageal cancer risk: assessment of susceptibility to DNA damage using comet assay.

Individuals' susceptibility to DNA damage could be identified by mutagen-challenged assays. We tested the hypothesis that susceptibility to DNA damage, measured by comet assay, may be associated with increased esophageal cancer (EC) risk. We recruited 102 subjects with previously untreated EC and 112 healthy controls. Baseline (untreated), benzo[a]pyrene diol epoxide (BPDE)-induced, and gamma-radiation-induced DNA damage were quantified by the Olive tail moment parameter. The mean tail moment was significantly higher in cases than in controls at baseline (case vs. control: 2.6 vs. 1.9, P < 0.01), after BPDE induction (case vs. control: 3.8 vs. 2.7, P < 0.01), and after gamma-radiation-induction (case vs. control: 5.0 vs. 3.8, P < 0.01). When data were dichotomized with the median values in the controls, a significantly increased risk for EC was observed for high baseline tail moment [odds ratio (OR) = 5.7, 95% confidence interval (CI) = 2.9-11.4], high BPDE-induced tail moment (OR = 5.8, 95% CI = 2.9-11.8), and high gamma-radiation-induced tail moment (OR = 4.6, 95% CI = 2.4-8.8). Further, the association between DNA damage and EC was stronger in never smokers than in ever smokers. Compared with subjects not sensitive to both mutagens, individuals sensitive to only one mutagen showed a 3.4-fold risk for EC and those sensitive to both mutagens showed an 8.7-fold risk for EC. Thus, we conclude that susceptibility to DNA damage as assessed by comet assay might help identify individuals with high EC risk.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed2003

Comet assay and flow cytometry analysis of DNA repair in normal and cancer cells treated with known mutagens with different mechanisms of action.

In order to determine differences in repair after treatment with DNA damaging agents, normal and cancer cells were selected for analysis of single strand breaks and DNA crosslinks using the Comet assay. Normal human lymphocytes, human colorectal adenocarcinoma SW620 cells, lung carcinoma A549, and H460 cell lines were exposed to an ethylating agent (ethylmethane sulfonate [EMS]), and a cross-linking agent (mitomycin C [MMC]). Differences in repair profiles of DNA damage demonstrated using the comet assay were observed in human lymphocytes and tumour cell lines with both mutagens. Results were also indicative that MMC repair is concentration-dependent. It was also apparent that normal cells repair DNA damage more readily than tumour cells. Repair also varied between different cell lines. To investigate the mechanistic differences of these two chemicals, flow cytometry studies were undertaken in tumour cells, namely cell cycle analysis and frequency of micronuclei induction (FMN). A G2M phase block was clearly evident following treatment with EMS at all concentrations tested. With MMC, an initial arrest of cells in G2M was accompanied by a build-up in S-phase over longer exposure periods. Also, at the highest mutagen doses there were different patterns of micronuclei induction. Thus, using the mutagens with different mechanisms of action highlighted the differences in repair patterns between normal and tumour cells.

Cell Cycle↗
PubMed2003

Oxygen-induced DNA damage in freshly isolated brain cells compared with cultured astrocytes in the Comet assay.

Brain cells are continuously exposed to reactive oxygen species generated by oxidative metabolism, and in certain pathological conditions defence mechanisms against oxygen radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important, therefore, to identify tools for the quantitative analysis of DNA damage in models of neurological disorders. The aim of this study was to compare the susceptibility of DNA to oxidative stress in cells freshly dissociated from the mouse brain, to that in cultured brain cells. Both primary cultures and a continuous cell line of astrocytes were considered. All cells were treated by xanthine/xanthine oxidase, a superoxide generator or hydrogen peroxide, applied alone or in the presence of the oxygen radical scavengers, superoxide dismutase, catalase, or ascorbic acid. DNA damage, quantified with the Comet assay, was consistent in all the different cell preparations exposed to oxidative stress, and was attenuated in similar ways by superoxide dismutase and catalase, scavengers of superoxide anion and hydrogen peroxide, respectively. The results with ascorbic acid were more variable, presumably because this compound may switch from anti- to pro-oxidant status depending on its concentration and other experimental conditions. Overall, similar responses were found in freshly dissociated and cultured brain cells. These results suggest that the Comet assay can be directly applied to cells freshly dissociated from the brain of rodents, including models of neurological disorders, such as stroke models and animals with targeted mutations that mimic human diseases.

Animals↗
PubMed2006

Comparative evaluation of genotoxicity of captan in amphibian larvae (Xenopus laevis and Pleurodeles waltl) using the comet assay and the micronucleus test.

Captan (N-trichloromethylthio-4-cyclohexene-1,2-dicarboximide) is a fungicide used to inhibit the growth of many types of fungi on plants used as foodstuffs. The toxic and genotoxic potentials of captan were evaluated with the micronucleus test (MNT; AFNOR,2000) and the comet assay (CA) using amphibian larvae (Xenopus laevis and Pleurodeles waltl). Acute toxicity results showed that captan was toxic (1) to Xenopus larvae exposed to from 2 mg/L to 125 or 62.5 microg/L, depending on the nature of the water [reconstituted water containing mineral salts or mineral water (MW; Volvic, Danone, France)] and (2) to Pleurodeles exposed to from 2 mg/L to 125 microg/L in both types of water. The MNT results obtained in MW showed that captan (62.5 microg/L) was genotoxic to Xenopus but not genotoxic to Pleurodeles at all concentrations tested. CA established that the genotoxicity of captan to Xenopus and Pleurodeles larvae depended on the concentration, the exposure times, and the comet parameters (tail DNA, TEM, OTM, and TL). The CA and MNT results were compared for their ability to detect DNA damage at the concentrations of captan and the exposure times applied. CA showed captan to be genotoxic from the first day of exposure. In amphibians, CA appears to be a sensitive and suitable method for detecting genotoxicity such as that caused by captan.

Amphibians↗
PubMed2002

Sister chromatid exchange rate and alkaline comet assay scores in patients with ovarian cancer.

OBJECTIVE: Sister chromatid exchange (SCE) frequencies were studied in patients with different types of ovarian malignancies and in healthy volunteers. The level of DNA damage in patients with ovarian malignancy and control subjects has also been studied by alkaline single cell gel electrophoresis (SCGE), also known as the comet assay. PATIENTS AND METHODS: Peripheral blood was collected from 30 patients after histological confirmation of malignancy and 20 healthy female volunteers. The cells were evaluated according to their grade of damage. RESULTS: We found that the sister chromatid exchange frequencies of cancer cases were significantly greater than that of controls (P < 0.001). The frequency of exchange in chromosomal groups A, B, and C, which include chromosomes 1-12, was higher than that of the other chromosomal groups in both groups. Comparison of the results of the alkaline comet assay in patient and control subjects showed a significant difference in the number of damaged cells. The frequency of limited migrated and extensive migrated cells in the women with ovarian malignancies was higher than that of control women (P < 0.001). CONCLUSIONS: SCE and SCGE can be used successfully to monitor DNA damage in women with ovarian cancer.

Adult↗
PubMed2000

Evaluation of the alkaline comet assay and urinary 3-methyladenine excretion for monitoring DNA damage in melanoma patients treated with dacarbazine and tamoxifen.

PURPOSE: To develop, using dacarbazine as a model, reliable techniques for measuring DNA damage and repair as pharmacodynamic endpoints for patients receiving chemotherapy. METHODS: A group of 39 patients with malignant melanoma were treated with dacarbazine 1 g/m(2) i.v. every 21 days. Tamoxifen 20 mg daily was commenced 24 h after the first infusion and continued until 3 weeks after the last cycle of chemotherapy. DNA strand breaks formed during dacarbazine-induced DNA damage and repair were measured in individual cells by the alkaline comet assay. DNA methyl adducts were quantified by measuring urinary 3-methyladenine (3-MeA) excretion using immunoaffinity ELISA. Venous blood was taken on cycles 1 and 2 for separation of peripheral blood lymphocytes (PBLs) for measurement of DNA strand breaks. RESULTS: Wide interpatient variation in PBL DNA strand breaks occurred following chemotherapy, with a peak at 4 h (median 26.6 h, interquartile range 14.75-40.5 h) and incomplete repair by 24 h. Similarly, there was a range of 3-MeA excretion with peak levels 4-10 h after chemotherapy (median 33 nmol/h, interquartile range 20.4-48.65 nmol/h). Peak 3-MeA excretion was positively correlated with DNA strand breaks at 4 h (Spearman's correlation coefficient, r=0.39, P=0.036) and 24 h (r=0.46, P=0.01). Drug-induced emesis correlated with PBL DNA strand breaks (Mann Whitney U-test, P=0.03) but not with peak 3-MeA excretion. CONCLUSIONS: DNA damage and repair following cytotoxic chemotherapy can be measured in vivo by the alkaline comet assay and by urinary 3-MeA excretion in patients receiving chemotherapy.

Adenine↗
PubMed2000

Comet assay as a tool to screen for mouse models with inherited radiation sensitivity.

Recent in vivo and in vitro data of patients analyzed for genetic susceptibility to radiation during cancer therapy have shown structural changes in the chromosomes to be prevalent both in the patients being treated and in their immediate family members. As structural changes in chromosomes frequently lead to activation of proto-oncogenes and elimination of tumor-suppressor genes, they represent important mechanisms for the initiation of DNA repair processes and tumorigenesis. With the exception of rare genetic syndromes such as AT (Ataxia telangiectasia) or NBS (Nijmegen Breakage Syndrome), the background for the inheritance of genetic susceptibility to radiation is unknown. Recently, a large-scale genetic screen of mouse mutants has been established within the German Human Genome Project (Hrabè de Angelis and Balling 1998). The goal of this ENU (ENU: ethylnitrosourea) mutagenesis screen is the generation of mutant mice that will serve as animal models for human diseases and genetic susceptibility. In order to fully utilize the potential of a genetic screen of this magnitude, in which exploration for genes responsible for genomic instability and radiation sensitivity is to occur, it is necessary to establish a simple assay system that is amenable to automation. Hence, we are using the single-cell gel electrophoresis (comet assay) to detect mouse mutants that display a genetic susceptibility to ionizing radiation. We have established the analysis parameters in the comet assay which are currently used to detect radiation-sensitive mouse mutants and to control the variance within the mouse population in the ENU screen. The assay can be used to isolate genes that are responsible for DNA repair and radiation sensitivity in mouse and human.

Animals↗
PubMed2005

Detection of genetic instability at HER-2/neu and p53 loci in breast cancer cells sing Comet-FISH.

A proportion of breast cancers acquire genetic alterations at 17q11.2-q12 (HER-2/neu), 20q13.2 (ZNF217 gene) and 17p13.1 (p53). We describe a unique technique (Comet-FISH) in which we documented relative genetic instability at p53 and HER-2/neu gene loci within a panel of malignant breast cancer cell lines (MCF-7; MDA-MB-468 and CRL-2336). Furthermore, Comet-FISH data were consistent with preferential repair of the p53 locus following gentoxic insult and suggest that this assay may be quite useful for the study of genetic instability.

Breast Neoplasms↗
PubMed2026

Comet assay analysis of multigenerational genomic instability (F0-F2) in Aedes aegypti exposed to gamma radiation in Sterile Insect Technique.

The use of irradiation in the Sterile Insect Technique (SIT) is a sustainable and environmentally friendly strategy for controlling Aedes aegypti populations by the release of sterile males. However, the potential toxic effects of radiation on mosquito genetic material, as well as the heritability of such damage, remain insufficiently understood. In this study, we evaluated gamma radiation-induced DNA damage (20, 30, 40, and 50 Gy) in male pupae (F0 generation) and assessed the persistence of these effects in subsequent generations (F1 and F2) using the comet assay in hemocytes. In the parental generation, a significant dose-response relationship was observed, with increasing radiation doses associated with higher damage index and damage frequency (p < 0.05). In the F1 generation, both larvae and adults exhibited significantly greater DNA damage than the control group, particularly at doses of 30 and 40 Gy, supporting the inheritance of radiation-induced genomic instability. In the F2 generation, genotoxic effects were attenuated, although residual damage remained detectable in adults, suggesting partial recovery of genomic stability, possibly influenced by DNA repair mechanisms and/or selective pressures. No viable offspring were obtained at 50 Gy, confirming the sterilizing efficacy of higher doses. Integration of comet assay results with micronucleus data and reproductive parameters reinforces the association between DNA damage, mutagenic effects, and reduced fertility. These findings indicate that radiation-induced genotoxic effects may persist beyond the irradiated generation but tend to decline across generations. Overall, this study provides insights into the balance between achieving sterility and preserving biological quality in SIT programs, contributing to optimizing radiation doses and enhancing the safety and efficacy of vector control strategies.

Comet assay↗
PubMed2004

Genotoxicant induced DNA damage and repair in early and late developmental stages of the grass shrimp Paleomonetes pugio embryo as measured by the comet assay.

In this study, data are presented which link frequency of DNA strand breaks and repair capability to developmental stage. Stages 4 and 7 embryos of the grass shrimp (Palaemonetes pugio) were exposed to various concentrations of benzo[alpha]pyrene (BalphaP), Cr(VI) and hydrogen peroxide. Following exposure, responses were measured as changes in hatching rates and DNA strand breaks (using the comet assay). The comet assay was modified by treatment of isolated nuclei with endonucleases which cleave DNA at oxidative lesions in DNA prior to electrophoresis. DNA repair was followed by transfer of toxicant exposed embryos to clean water and periodic determination of strand breaks. DNA strand breaks were higher in stage 7 embryos than in stage 4 embryos after exposure to the same concentration of different genotoxicants. However, when samples were treated with endonucleases to measure oxidative lesions, the total amount of DNA damage between stages 4 and 7 were similar. After toxicant exposure and transfer to clean water, DNA strand breaks in stage 7 embryos returned to background levels more rapidly than in stage 4 embryos. Similarly, samples treated with endonucleases during DNA repair studies showed that oxidative lesions were repaired more rapidly in stage 7 than in stage 4. These findings suggest that because of rapid DNA repair in late embryo stages that early embryo stages are more likely to have developmental effects after genotoxicant exposure.

Animals↗
PubMed2004

Application of the comet and micronucleus assays to the detection of B[a]P genotoxicity in haemocytes of the green-lipped mussel (Perna viridis).

Green-lipped mussels (Perna viridis) were exposed to water-borne benzo[a]pyrene (B[a]P) at nominal concentrations of 0, 0.3, 3 and 30 microg l(-1) for up to 12 days, and both the relative levels of DNA strand breaks (assessed using an alkaline comet assay) and the proportion of micronucleus (MN) formation were monitored in mussel haemocytes at days 0, 1, 3, 6 and 12. The results of the comet assay indicated that an increase in the proportion of strand breaks occurred generally with increasing B[a]P concentration, but a significant decrease in the levels of DNA damage was observed after exposure for 12 days at all concentrations tested, suggesting that the patterns of changes in the levels of DNA strand breakage can be explained by the threshold dependent DNA repair theory. Moreover, the relatively slow development and recovery of the DNA damage response in mussel haemocytes in comparison with previous findings utilizing P. viridis hepatopancreas suggests that the response of DNA alteration upon exposure to B[a]P may be tissue-specific in this species. Monitoring the frequency of micronucleus development in mussel haemocytes indicated both dose- and time-response relationships within the exposure period. Furthermore, the levels of DNA strand breakage correlated well with the levels of micronucleus induction, suggesting a possible cause and effect relationship between the two damage types. We suggest that DNA strand breakage and micronucleus formation in mussel haemocytes can potentially be used as convenient biomarkers of exposure to genotoxicants in the marine environment.

Analysis of Variance↗
PubMed2005

Cytotoxic and genotoxic effects of resin monomers in human salivary gland tissue and lymphocytes as assessed by the single cell microgel electrophoresis (Comet) assay.

Malignant tumors of the three major pairs and the numerous minor salivary glands in humans are rare, and little is known about their various etiologies. Considering the fact that resin monomers from dental restorative materials are released into the saliva and diffuse into the tooth pulp or gingiva, mucosa, and salivary glands, this may potentially contribute to tumorigenesis. Resin monomers may also be reabsorbed and reach the circulating blood as well. Whereas the cytotoxic potential of some components has been clearly documented, data on genotoxicity in human target cells require further investigation. In the present study, genotoxic and cytotoxic effects of three common methacrylates are investigated in human samples of salivary glands and peripheral lymphocytes. The Comet assay was used to quantify DNA single strand breaks, alkali labile and incomplete excision repair sites in salivary gland probes and lymphocytes of 10 volunteers. The xenobiotics investigated were triethyleneglycoldimethacrylate (TEGDMA), urethanedimethacrylate (UDMA), and 2-hydroxyethylmethacrylate (HEMA), with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and dimethyl sulfoxide (DMSO) as controls. DNA migration was analyzed using the tail moment according to Olive (OTM). Cytotoxicity was monitored using trypan blue staining. With TEGDMA concentrations at 10(-5)m (10(-3)m), UDMA at 10(-7)m (10(-7)m), and HEMA at 10(-3)m (10(-5)m) significant enhancements of DNA migration were achieved in tissue cells (lymphocytes) as compared to the negative controls. At higher concentrations of up to 2.5x10(-2)m, induced DNA migration was expressed by OTM at 10.7 for TEGDMA in tissue cells (8.7 in lymphocytes), 10.5 for UDMA (6.4), and 9.7 for HEMA (6.1). The viability of the cell systems was not affected as concerns the threshold level for the assay of 75% viable cells except for the highest concentration tested for TEGDMA and UDMA in tissue cells. At higher concentration levels, all tested substances induced significant enhancement of DNA migration in the Comet assay as a possible sign for genotoxic effects in human salivary glands and lymphocytes. These data add to the results of prior studies in human peripheral lymphocytes and give evidence of a possible risk factor for tumor initiation in human salivary glands.

Aged↗
PubMed2004

The comet assay differentiates efficiently and rapidly between genotoxins and cytotoxins in quiescent cells.

Our main aim was to establish the efficiency of the single cell electrophoresis technique for differentiating between drugs that bind DNA and those that do not. The alkaline comet assay was used to test the responses of human leukocytes (quiescent cells) to damage induced by reportedly genotoxic and reportedly cytotoxic agents. Incubation of G0 leukocytes for 1 h with the genotoxic agents camptothecin and actinomycin C provoked DNA migration, observed as comet figures. On the other hand, when cells were treated with the cytotoxic agents cordycepin, fluorodeoxyuridine and puromycin, the leukocyte nuclei were indistinguishable from those of untreated cells. In addition, we have developed a rapid method using non-proliferating cells that requires neither culture nor lymphocyte isolation. This method promises to be useful as a rapid in vitro screening assay.

Antimetabolites, Antineoplastic↗
PubMed2005

Exchange of beta-blockers in heart failure patients. Experiences from the poststudy phase of COMET (the Carvedilol or Metoprolol European Trial).

BACKGROUND: The Carvedilol or Metoprolol European Trial (COMET) reported a significant survival benefit for carvedilol, a beta1-, beta2- and alpha1-blocker, vs. metoprolol tartrate, a beta1-selective blocker, in patients with mild-to-severe chronic heart failure (CHF). Patients on treatment with metoprolol might benefit from switching to carvedilol. AIM: To investigate the safety and tolerability of switching beta-blockers in CHF. METHODS: At the end of COMET, the Steering Committee recommended that study medication was stopped without unblinding, and patients were commenced on open-label beta-blockade at a dose equivalent to half the dose of blinded therapy, with subsequent titration to target or maximum tolerated dose. Patients were followed for 30 days. RESULTS: 1321 out of 1440 patients were transitioned to open-label treatment (76.8% to carvedilol). Serious adverse and CHF-related events were respectively 9.4% and 4.7% in those switching from carvedilol to metoprolol and 3.1% and 1.5% in patients switching from metoprolol to carvedilol. Patients who switched from carvedilol to metoprolol showed the highest mortality or hospitalisation rate (12.3%) in comparison with those who switched from metoprolol to carvedilol (3.1%, p<0.001) or who stayed on the same drug (carvedilol: 2.5%, p<0.001; metoprolol: 4.2%, p=0.04). Reducing the initial dose of the second beta-blocker maximised the safety of this strategy. Event rate was higher in patients with more severe heart failure and in those withdrawing from beta-blockade. CONCLUSION: Our data show that switching beta-blockers is a practical, safe and well-tolerated strategy to optimise treatment of CHF. Patients who switched to carvedilol showed the lowest rate of adverse events. A closer clinical monitoring is recommended during transition in high-risk patients.

Adrenergic beta-Antagonists↗
PubMed2004

Increased frequency of sister-chromatid exchange and altered alkaline comet assay scores in superovulation cycles for unexplained infertility.

OBJECTIVE: Sister-chromatid exchange analysis (SCE) and alkaline comet assay measure and analyze DNA damage in mammalian cells. This study assesses whether ovulation induction agents increase DNA damage in the lymphocytes of infertile women undergoing superovulation. STUDY DESIGN: Prospective case control study in a university based hospital. Baseline and hCG day peripheral blood samples were withdrawn from 20 women with undergoing superovulation for unexplained infertility and baseline and luteinizing hormone (LH) peak day samples were also withdrawn from another 20 infertile women with unexplained infertility. RESULTS: There was increased SCE frequency and DNA damage determined by comet assay on the hCG day compared to the basal state. The SCE increase was correlated with the hCG day estradiol (E2) but not with ampoules of follicular stimulating hormone (FSH). The SCE frequency was also increased naturally ovulating women; however this was significantly less than that in FSH receiving women. CONCLUSION: Increased DNA damage may indicate for increased potential for malignancies after superovulation.

Adult↗
PubMed2005

In vivo DNA damaging potential of sanguinarine alkaloid, isolated from argemone oil, using alkaline Comet assay in mice.

Consumption of mustard oil contaminated with argemone oil is well known to cause clinical manifestation referred to as "Epidemic Dropsy". Our prior studies have shown that argemone oil produces genotoxic effects in mice [Ansari, K.M., et al., 2004. Int. J. Cancer 112, 890]. Since, sanguinarine alkaloid is the major component of argemone oil, the in vivo DNA damaging potential of the isolated alkaloid was investigated in blood and bone marrow cells of mice using alkaline Comet assay. Swiss albino male mice were given single intraperitoneal administration of 1.35, 2.70, 5.40, 10.80 and 21.60 mg sanguinarine alkaloid/kg b wt., while controls were treated with saline in the same manner. The results revealed a dose dependent increase in DNA damage in blood and bone marrow cells following 24 h treatment of sanguinarine alkaloid. All the three parameters of Comet assay including olive tail moment (OTM), tail length and tail DNA showed significant (p<0.05) increases in blood and bone marrow cells at respective doses of 10.80 and 5.40 mg alkaloid/kg b wt. However, some of the parameters were significantly increased even at lower doses of sanguinarine alkaloid (2.70 mg/kg b wt.). The frequency of cells exhibiting greater DNA damage were found to be increased by sanguinarine alkaloid in a concentration dependent manner. These results indicate that single exposure of sanguinarine alkaloid causes DNA damage in blood and bone marrow cells of mice, which could be responsible for the genotoxicity of argemone oil.

Alkaloids↗