RESUMEN
Results: Road tunnel construction workers revealed higher frequencies of cells with genotoxic damage (i.e., MN and NBUD). MN and NBUD resulted to be Poisson distributed and counts of these genotoxicity biomarkers were then analysed by Poisson regression. The frequency ratio (FR) for MN was 1.31 (95% CI: 0.84-2.04), with an increase in the exposed subjects; this finding, though indicating a higher genotoxic risk in the exposed subjects, did not reach statistical significance. On the other hand, the FR for NBUD was 3.49 (95% CI: 1.86-6.56), with a statistically significant increased risk of chromosomal damage. Even the frequencies of binucleated cells (a marker of cell proliferation) and pyknotic cells (a cell death biomarker) were significantly higher in tunnel workers. Introduction: Tunnel construction workers are exposed to complex mixtures of toxic agents, some of which are known to be genotoxic. The aim of this study was to evaluate the genotoxic risk in this occupational setting by comparing tunnel workers with a control group for frequencies of nuclear aberrations in oral exfoliated cells. Methods: To evaluate the genotoxic effects of tunnel air pollutants, we conducted a cross-sectional, molecular epidemiological study (35 tunnel workers and 35 healthy controls) using the buccal micronucleus cytome assay. A questionnaire was administered to obtain information about demographic variables, lifestyle, dietary habits, anthropometric data, and occupational history. Buccal mucosa cells were collected by scraping the buccal mucosa with a small-headed toothbrush. Coded slides were examined blind by trained scorers for micronuclei (MN), nuclear buds (NBUD), and other nuclear abnormalities. Conclusions: Our observations provide further knowledge and understanding of the occupational hazards of tunnel workers and confirm the complexity of effects (cytotoxic and genotoxic) probably induced by fumes and dust produced in underground operations.
Asunto(s)
Monitoreo Biológico , Exposición Profesional , Estudios Transversales , Análisis Citogenético , Daño del ADN , Humanos , Pruebas de Micronúcleos , Exposición Profesional/efectos adversosRESUMEN
In tunnel construction workers, occupational exposure to dust (alpha-quartz and other particles from blasting), gases (nitrogen dioxide, NO(2)), diesel exhausts, and oil mist has been associated with lung function decline, induction of inflammatory reactions in the lungs with release of mediators that may influence blood coagulation, and increased risk of chronic obstructive pulmonary disease. The present molecular epidemiology study was designed to evaluate whether occupational exposure to indoor pollutants during road tunnel construction might result in genotoxic effects. A study group of 39 underground workers and a reference group of 34 unexposed subjects were examined. Primary and oxidative DNA damage, sister-chromatid exchanges (SCE), and micronuclei (MN) were measured in peripheral blood cells. The possible influences of polymorphisms in gene encoding for CYP1A1 and GSTM1 xenobiotic-metabolizing enzymes were also investigated. Exposure assessment was performed with detailed interviews and questionnaires. There were no significant differences in the level of primary and oxidative DNA damage and frequency of SCE between the tunnel workers and controls, whereas the frequency of MN showed a significant increase in exposed subjects compared to controls. No effects of CYP1A1 or GSTM1 variants were observed for the analyzed biomarkers. Since MN in peripheral blood lymphocytes are recognized as a predictive biomarker of cancer risk within a population of healthy subjects, the genotoxic risk of occupational exposure to various indoor environmental pollutants during road tunnel construction cannot be excluded by this biomonitoring study.
Asunto(s)
Contaminantes Ocupacionales del Aire/efectos adversos , Citocromo P-450 CYP1A1/genética , Daño del ADN/efectos de los fármacos , Glutatión Transferasa/genética , Exposición Profesional/efectos adversos , Polimorfismo Genético , Cuarzo/efectos adversos , Intercambio de Cromátides Hermanas/efectos de los fármacos , Transportes , Adulto , Contaminantes Ocupacionales del Aire/sangre , Estudios de Casos y Controles , Ensayo Cometa/métodos , Citocromo P-450 CYP1A1/efectos de los fármacos , Polvo , Glutatión Transferasa/efectos de los fármacos , Humanos , Italia , Masculino , Pruebas de Micronúcleos/métodos , Encuestas y CuestionariosRESUMEN
In the last few years chlorine dioxide has been increasingly used for disinfecting drinking water in many countries. Although it does not react with humic substances, chlorine dioxide added to water is reduced primarily to chlorite and chlorate ions, compounds that are under investigation for their potential adverse effects on human health. The aim of this research was to study the genotoxicity of chlorite and chlorate and their mixtures. The end-points included two plant tests (chromosomal aberration test in Allium cepa and micronucleus assay in Tradescantia, carried out at different times of exposure) and two genotoxicity tests in human HepG2 cells (comet assay and cytokinesis-blocked micronucleus test). Preliminary toxicity tests were carried out for both plant and HepG2 assays. The results showed that chlorite and chlorate are able to induce chromosomal damage to plant systems, particularly chromosomal aberrations in A. cepa root tip cells, even at concentrations lower than the limit established by Italian normative law and WHO guidelines. In HepG2 cells increased DNA damage was only observed for chlorate at the lowest concentration. No increase in micronuclei frequency was detected in any of the samples tested in human HepG2 cells.
Asunto(s)
Cloratos/toxicidad , Cloruros/toxicidad , Daño del ADN , Bioensayo/métodos , Línea Celular Tumoral , Cromosomas de las Plantas/efectos de los fármacos , Cromosomas de las Plantas/genética , Ensayo Cometa/métodos , Humanos , Pruebas de Micronúcleos/métodos , Pruebas de Mutagenicidad/métodos , Cebollas/efectos de los fármacos , Cebollas/genética , Tradescantia/efectos de los fármacos , Tradescantia/genéticaRESUMEN
We carried out an integrated environmental/biological monitoring program to evaluate cancer hazards among metal industry workers exposed to cutting fluids. Several cutting fluids were sampled according to response to a semiquantitative nitrite rapid test in metal factories in central Italy. The nitrite-positive samples were analyzed for nitrite and nitrosodiethanolamine (NDELA) content and mutagenic activity. The nitrite-negative samples were analyzed only for mutagenicity. Of the total samples, 20.6% were nitrite positive, and all contained NDELA. However, nitrite content was not quantitatively predictive of the NDELA content, which varied enormously among samples (0.3-1900 mg/kg). Nitrite-negative samples were always nonmutagenic. Mutagenicity was found in half the NDELA-containing samples but was not related to nitrite or NDELA content. Nitrite screening of cutting fluids in the field is an interesting method for identifying samples that potentially contain NDELA and other unknown mutagens and, when performed with short-term mutagenicity tests, nitrite screening seems to be a valid tool by which industrial managers and health officers could minimize the health hazards associated with occupational exposure to cutting fluids.
Asunto(s)
Dietilnitrosamina/análogos & derivados , Monitoreo del Ambiente/métodos , Metalurgia/métodos , Mutágenos/análisis , Nitritos/análisis , Dietilnitrosamina/análisis , Humanos , Pruebas de Mutagenicidad , Salud LaboralRESUMEN
Biological monitoring of occupational hazards was performed in workers using cutting fluids containing N-nitrosodiethanolamine (NDELA). The study involved a group of 25 male subjects from some metal factories in central Italy who used cutting fluids with an NDELA content of > or = 5 mg/l (high-exposure group) and a group of 37 males exposed to cutting fluids with an NDELA content < 5 mg/l (low-exposure group). For comparison, we recruited a control group consisting of 37 subjects living in the same area. For all subjects, internal dose (urinary excretion of NDELA, mutagens, and thioethers), early biological effects (sister chromatid exchanges in blood peripheral lymphocytes), and urinary excretion of D-glucaric acid (DGA) as an endpoint product in the glucuronidation pathway were assessed. The results showed that only the workers using cutting fluids with NDELA concentrations of > or = 5 mg/l excreted trace amounts of NDELA in their urine. Urine excretion of mutagens was similar in the two exposure groups and in the controls. High-exposure subjects had a higher mean value of urinary thioethers than low-exposure and control subjects, but no differences were found in urinary DGA or lymphocyte sister chromatid exchange among the three groups. Smoking status increased the mean values of all the biomarkers, and coffee drinking was associated with urinary DGA excretion.
Asunto(s)
Carcinógenos/metabolismo , Dietilnitrosamina/análogos & derivados , Monitoreo del Ambiente , Exposición Profesional , Adulto , Carcinógenos/efectos adversos , Dietilnitrosamina/efectos adversos , Dietilnitrosamina/metabolismo , Dietilnitrosamina/orina , Ácido Glucárico/orina , Humanos , Masculino , Metalurgia , Persona de Mediana Edad , Mutágenos , Intercambio de Cromátides Hermanas , Sulfuros/orinaRESUMEN
Biological monitoring of genotoxic hazard in the rubber industry was performed in 19 male workers and 20 age-matched controls in a local health unit in northern Italy. Peripheral blood lymphocytes were analyzed for the presence of DNA damage (single-cell microgel-electrophoresis, or comet assay) and for cytogenetic parameters (sister chromatid exchanges and micronuclei frequency, and proliferative rate index). The following bioassays were performed in urine samples: a) mutagenicity test and concentration of thioethers as markers of exposure, and b) excretion of D-glucaric acid and 6-beta-hydroxycortisol (related to 17-hydroxycorticosteroid excretion) as indicators of the inductive status of the microsomal enzyme system (phase-I). The exposed subjects showed statistically higher mean values of 17-hydroxycorticosteroids and micronuclei and lower values of 6-beta-hydroxycortisol than controls, when taking cigarette smoking into account. The comet assay showed higher values for migration distance in exposed subjects than controls, although the differences were not significant at a p-value of 0.05. These findings suggest that industrial exposure in the rubber processing industry may cause genetic damage and may modify the activity level of some enzymes; these results should be considered with caution due to the small number of subjects enrolled.
Asunto(s)
Mutágenos/análisis , Exposición Profesional , Adulto , Biomarcadores , Aberraciones Cromosómicas , Daño del ADN , Monitoreo del Ambiente , Ácido Glucárico/orina , Humanos , Hidrocortisona/análogos & derivados , Hidrocortisona/orina , Industrias , Linfocitos/efectos de los fármacos , Masculino , Pruebas de Micronúcleos , Exposición Profesional/efectos adversos , Goma , Intercambio de Cromátides Hermanas/efectos de los fármacos , Fumar/efectos adversos , Sulfuros/orinaRESUMEN
A petroleum pitch sample collected in a carbon electrode factory was studied using a series of in vivo assays for genotoxicity and enzymatic induction capability. Rats were treated with the petroleum derivative in three doses: 100, 50, and 10 mg/kg body weight. The treatment produced a rapid excretion of mutagenic substances in the urines of the first 24 hr only in rats treated with high doses (100 and 50 mg/kg). No faecal mutagenic activity was observed. Analyses of urinary thioethers showed that urinary metabolites derived from the compounds present in the pitch-sample at the lowest dose-administered (10 mg/kg) were eliminated primarily as cysteine conjugates. The pitch sample was found to be a good inducer of pulmonary and hepatic aryl hydrocarbon hydroxylase, especially after a 50 mg/kg dose. Urinary D-glucaric acid content was always statistically increased in treated animals compared with controls, confirming the enzymatic induction activity. Hepatic glutathione-S-transferase activity increased following treatment with 50 and 10 mg/kg doses.
Asunto(s)
Monitoreo del Ambiente/métodos , Mutágenos/orina , Petróleo/toxicidad , Animales , Hidrocarburo de Aril Hidroxilasas/biosíntesis , Biomarcadores/orina , Inducción Enzimática/efectos de los fármacos , Heces/análisis , Ácido Glucárico/orina , Glutatión Transferasa/biosíntesis , Hígado/efectos de los fármacos , Hígado/enzimología , Pulmón/efectos de los fármacos , Pulmón/enzimología , Masculino , Pruebas de Mutagenicidad , Ratas , Ratas Endogámicas , Sulfuros/orinaRESUMEN
Deltamethrin, a synthetic dibromo-pyrethroid insecticide, is extensively used in agriculture, forestry and in household products because of its high activity against a broad spectrum of insect pests (both adults and larvae), its low animal toxicity and its lack of persistence in the environment. Data on the genotoxicity and carcinogenicity of deltamethrin are rather controversial, depending on the genetic system or the assay used. The aim of this study was to further evaluate the potential genotoxic activity of deltamethrin. The in vitro genotoxicity of deltamethrin has been evaluated by assessing the ability of the insecticide to damage DNA (as evaluated using the single-cell microgel-electrophoresis or 'comet' assay) or induce sister-chromatid exchanges (SCE) and micronuclei (MN) in human peripheral blood leukocytes. All treatments were conducted with and without the presence of an external bioactivation source (+/- S9mix). The results indicate that deltamethrin, in the presence of metabolic activation (+ S9mix), is able to induce DNA damage (double- and single-strand breaks, alkali-labile sites and open excision repair sites) as revealed by the increasing tail moment values observed with increasing doses. The frequency of SCE and MN were not statistically increased in deltamethrin-treated cells as compared to controls, both with and without S9mix. However, lower deltamethrin doses were tested, as compared to 'comet' assay, because of cytotoxicity.
Asunto(s)
Daño del ADN/efectos de los fármacos , Insecticidas/toxicidad , Leucocitos/efectos de los fármacos , Piretrinas/toxicidad , Intercambio de Cromátides Hermanas/efectos de los fármacos , Adulto , Células Cultivadas/efectos de los fármacos , Electroforesis en Gel de Agar , Humanos , Procesamiento de Imagen Asistido por Computador , Insecticidas/metabolismo , Leucocitos/metabolismo , Masculino , Pruebas de Micronúcleos , Microsomas Hepáticos , Nitrilos , Piretrinas/metabolismoRESUMEN
The ureic herbicide linuron [3-(3, 4-dichlorophenyl)-1-methoxy-1-methylurea] (CAS 330-55-2) was investigated for genotoxicity in a series of in vivo experiments. Since human exposure to herbicides is not only to the active principles, but also to all the chemicals present in the commercial formulation, we tested both pure and commercial linuron. Groups of rats were treated with gavage containing different doses of the herbicide (pure compound or commercial formulation) for 14 days. The doses were 150, 300 and 450 mg/kg b.wt. for the pure compound and 315.8, 631.6 and 947.4 mg/kg b.wt. for the commercial formulation (47.5% of linuron). Faeces and urine were collected at regular intervals. Urine specimens were analysed for their mutagenic metabolites, thioethers and D-glucaric acid content. Faeces extracts were tested for mutagenicity. Linuron's ability to cause DNA damage and cytogenetic effects was also investigated after treating groups of rats once with different doses of pure or commercial linuron. DNA single-strand breaks were assessed in rat liver using the alkaline elution technique and the single-cell microgel electrophoresis assay (SCGE: 'comet' assay), and in rat testes cells with the SCGE assay. Micronuclei induction was analysed in rat bone marrow erythrocytes. Results obtained were mainly negative when the excretion of mutagenic metabolites in urine and faeces of animals treated with the pure compound or with the linuron-based commercial formulation were monitored, whereas an increase in the urinary excretion of thioethers and D-glucaric acid was observed in rats treated with the commercial formulation. No increase in the frequency of micronucleated polychromatic erythrocytes was observed in the treated animals. However, linuron affected the viability of hepatocytes isolated from animals treated with higher doses. This cytotoxicity was accompanied by the induction of DNA single-strand breaks in the liver, as seen by the alkaline elution assay. The potential of pure linuron to induce in vivo DNA damage was confirmed with the microgel-electrophoresis technique ('comet' assay). Cytotoxicity was also seen in rat testes cells. However, no indication of DNA damage was visible.
Asunto(s)
Daño del ADN/efectos de los fármacos , Herbicidas/toxicidad , Linurona/toxicidad , Hígado/efectos de los fármacos , Administración Oral , Animales , Heces/química , Ácido Glucárico/orina , Herbicidas/administración & dosificación , Herbicidas/orina , Linurona/administración & dosificación , Linurona/orina , Masculino , Micronúcleos con Defecto Cromosómico/efectos de los fármacos , Pruebas de Micronúcleos , Pruebas de Mutagenicidad , Ratas , Ratas Wistar , Salmonella typhimurium/efectos de los fármacos , Salmonella typhimurium/genética , Sulfuros/orina , Testículo/efectos de los fármacosRESUMEN
The effect of the ureic herbicide Linuron [3-(3,4-dichlorophenyl)-1-methoxy-1-methylurea] on the levels of some hepatic xenobiotic metabolizing enzymes was studied in rats. The cytochrome P450-dependent monooxigenase activities of aryl hydrocarbon hydroxylase (AHH) and of aminopyrine N-demethylase (APD) were measured in rat livers after a 14-d treatment by gavage with Linuron. AHH was employed as a marker of the catalytic activity of P450IA1 and APD as a marker of the catalytic activity of P450IIB1/2. Furthermore, the enzymatic activities of the cytosolic via glutathione detoxifying enzymes glutathione peroxidase and glutathione S-transferase were assessed. Three doses of Linuron (both as pure compound and as commercial preparation) were tested. The doses tested were 150, 300, and 450 mg/kg body weight for the pure compound and 315.8, 631.6, and 947.4 mg/kg for the commercial preparation. Differences were found in the relative liver weight only in rats treated with the commercial formulation. The aryl hydrocarbon hydroxylase activity was increased with all the tested doses of pure and commercial Linuron. A reduction in the aminopyrine N-demethylase activity was noted for the highest dose of pure Linuron, whereas an increment in this activity was observed for all the doses of the commercial preparation tested. The activity of glutathione peroxidase was not affected by treatment with the pure product; however, an increment in activity was observed at all the tested doses of the commercial preparation. The glutathione S-transferase activity was reduced in both cases.
Asunto(s)
Inducción Enzimática/efectos de los fármacos , Linurona/farmacología , Aminopirina N-Demetilasa/biosíntesis , Aminopirina N-Demetilasa/efectos de los fármacos , Animales , Hidrocarburo de Aril Hidroxilasas/biosíntesis , Hidrocarburo de Aril Hidroxilasas/efectos de los fármacos , Glutatión Peroxidasa/biosíntesis , Glutatión Peroxidasa/efectos de los fármacos , Glutatión Transferasa/biosíntesis , Glutatión Transferasa/efectos de los fármacos , Masculino , Ratas , Ratas WistarRESUMEN
The objective of this article is to assess whether occupational exposure to anesthetics increases genotoxic risk. We investigated two cytogenetic biomarkers, sister chromatid exchanges (SCE) and micronuclei (MN), in the peripheral blood lymphocytes of 46 anesthesiologists (24 men), working in operating rooms and mostly exposed to enfluorane and nitrous oxide, and 66 controls (35 men), not exposed to chemicals and living in the same area. Contrary to what was expected, a lower frequency of SCE was found in male anesthesiologists than in controls. Smoking status was found to be positively associated with SCE frequency in each group, while no relation to age was evident. On the contrary, MN frequency was significantly higher in female, but not male, anesthesiologists than in controls. Age and smoking status did not modify the association. No relationship between MN frequency and duration of employment was found in anesthesiologists. Smoking status and mean number of cigarettes smoked per day in smokers were not associated with MN frequency in either anesthesiologists or in controls. MN analysis seems to be a sensitive index of possible genotoxic effects of occupational exposure to anesthesiologists, and women appear to be more susceptible to these effects than men.
Asunto(s)
Contaminantes Ocupacionales del Aire/efectos adversos , Anestésicos por Inhalación/efectos adversos , Enflurano/efectos adversos , Linfocitos/efectos de los fármacos , Micronúcleos con Defecto Cromosómico/efectos de los fármacos , Óxido Nitroso/efectos adversos , Quirófanos , Intercambio de Cromátides Hermanas/efectos de los fármacos , Adulto , Anciano , Femenino , Humanos , Exposición por Inhalación , Masculino , Micronúcleos con Defecto Cromosómico/genética , Persona de Mediana Edad , Caracteres Sexuales , Intercambio de Cromátides Hermanas/genética , FumarRESUMEN
The frequency of sister chromatid exchanges (SCE) and micronuclei in peripheral blood lymphocytes was evaluated in 48 agricultural workers and 50 control subjects living in central Italy. No difference in SCE frequency was found between the control and the exposed populations with respect to age, smoking habits, and duration of exposure, although smokers, both farmers and controls, had a higher SCE frequency than nonsmokers. However, the comparison of proliferative rate index values found in the two groups revealed a significant decrease in the activation capability of lymphocytes in the pesticide-exposed workers, probably related to the toxic properties of chemicals to which the farmers were exposed. On the contrary, the analysis of micronuclei frequency indicated that there were differences between the exposed and control subjects with respect to smoking habits, age, and duration of exposure. Our results indicate that, in the study population occupationally exposed to a complex mixture, including insecticides, fungicides, and herbicides, there is clear, although slight, evidence of clastogenic activity in peripheral blood lymphocytes but no corresponding effects on SCE induction. Moreover, our data show clear evidence of cell proliferation delay relatable to chemical compounds used in agriculture.
Asunto(s)
Enfermedades de los Trabajadores Agrícolas/etiología , Citogenética/métodos , Exposición Profesional/efectos adversos , Plaguicidas/toxicidad , Adulto , Anciano , Daño del ADN/genética , Evaluación de Medicamentos/métodos , Humanos , Italia/epidemiología , Activación de Linfocitos/efectos de los fármacos , Linfocitos/efectos de los fármacos , Masculino , Micronúcleos con Defecto Cromosómico/genética , Persona de Mediana Edad , Intercambio de Cromátides Hermanas/genética , Fumar/efectos adversosRESUMEN
Compounds possessing antimutagenic properties (polyphenols, tannins, vitamins, etc.) have been identified in fruits, vegetables, spices, and medicinal plants. Terminalia arjuna (Combretaceae), a tropical woody tree occurring throughout India and known locally as Kumbuk, is a medicinal plant rich in tannins and triterpenes that is used extensively in Ayurvedic medicine as a cardiac tonic. The aim of the present collaborative work was to test six solvent extracts from the bark of Terminalia arjuna for antigenotoxic activity using in vitro short-term tests. Terminalia arjuna extracts were obtained by sequential extraction using acetone, methanol, methanol + HCl, chloroform, ethyl acetate, and ethyl ether. The antigenotoxic properties of these extracts were investigated by assessing the inhibition of genotoxicity of the directacting mutagen 4-nitroquinoline-N-oxide (4NQO) using the "comet" assay and the micronucleus (MN) test. Human peripheral blood leukocytes were incubated with different concentrations of the six extracts (from 5 to 100 microg/ mL) and with 4NQO (1 and 2 microg/mL, for the "comet" assay and MN test, respectively). Each extract/4NQO combination was tested twice; in each experiment, positive control (4NQO alone) and negative control (1% DMSO) were set. "Comet" assay results showed that acetone and methanol extracts were highly effective in reducing the DNA damage caused by 4NQO, whereas the acidic methanol, chloroform, ethyl acetate, and ethyl ether extracts showed less marked or no antigenotoxic activity. In the MN test, a decrease in 4NQO genotoxicity was observed by testing this mutagen in the presence of acetone, methanol, chloroform, and ethyl acetate extracts, even though the extent of inhibition was not always statistically significant.
Asunto(s)
Antimutagênicos/farmacología , Daño del ADN/efectos de los fármacos , Extractos Vegetales/farmacología , Terminalia/química , 4-Nitroquinolina-1-Óxido/toxicidad , Ensayo Cometa , Medicina Ayurvédica , Pruebas de Micronúcleos , Mutágenos/toxicidad , Extractos Vegetales/química , Quinolonas/toxicidad , Solventes/químicaRESUMEN
The generation, transmission (e.g. power lines, transformers, service wires, and electrical panels), and use (e.g. home appliances, such as electric blankets, shavers, and televisions) of electrical energy is associated with the production of weak electric and magnetic fields (EMF) which oscillate 50 (Europe) or 60 (USA) times per second (power-line frequency), falling in the extremely-low frequency (ELF) region of the electromagnetic spectrum. Epidemiological reports suggest a possible association between exposure to ELF-EMF and an increased risk of cancer (e.g. childhood acute leukaemia). Benzene is an established human leukomogen. This xenobiotic, which is unlikely to be the ultimate carcinogen, is metabolized in the liver to its primary metabolite phenol, which is hydroxylated to hydroquinone (1,4-benzenediol) and 1,2,4-benzenetriol. In this in vitro approach, to test the genotoxic and / or co-genotoxic potency of ELF-EMF, the cytokinesis block micronucleus (MN) method with Jurkat cells has been used. A 50 Hz magnetic field (MF) of 5 mT field strength was applied for different length of time (from 1 to 24 h), either alone or with benzene, 1,4-benzenediol, or 1,2,4-benzenetriol. Our preliminary results show that, after 24 h exposure, the frequency of micronucleated cells in MF-exposed cultures is 1.9 fold higher than in sham-exposed (control) cultures. Benzene exposure does not show any cytogenetic activity, whereas 1,4-benzenediol or 1,2,4-benzenetriol alone significantly affect the number of MN in Jurkat cells, as compared to untreated cultures. Moreover, co-exposure to ELF-MF does not seem to affect the frequency of micronuclei induced by benzene, 1,4-benzenediol, or 1,2,4-benzenetriol.
Asunto(s)
Benceno/toxicidad , Campos Electromagnéticos/efectos adversos , Hidroquinonas/toxicidad , Micronúcleos con Defecto Cromosómico/efectos de los fármacos , Micronúcleos con Defecto Cromosómico/efectos de la radiación , Humanos , Células Jurkat , Pruebas de Micronúcleos , Índice Mitótico , Factores de TiempoRESUMEN
Terbutryn is a widely used preemergence and postemergence s-triazine herbicide. This pesticide is used in agriculture as a control agent for most grasses and many annual broadleaf weeds in cereal and legume fields, and under fruit trees. Unexpectedly, this compound was found to persist in the environment (240 and 180 days in pond and river sediment, respectively) and to have the tendency to move from treated soils to water compartments through water runoff and leaching. However, only scant information is available about the genotoxic properties of terbutryn. In the present in vitro study, we investigated the relationship between cytogenetic damage, as evaluated in the sister-chromatid exchange (SCE) assay and the micronucleus (MN) test, and primary DNA damage (as evaluated by the "comet" assay). Cytogenetic and primary DNA damage were recorded in vitro in freshly isolated human peripheral blood leukocytes. Our results showed that the tested compound failed to produce any significant increases in SCE or MN, neither in the absence nor in the presence of S9-mix. However, terbutryn was found to induce primary DNA damage, more pronounced without S9 mix, even though in the absence of a clear trend for dose-dependence and in the presence of a concomitant mild cytotoxic effect.
Asunto(s)
Daño del ADN/efectos de los fármacos , Herbicidas/toxicidad , Pruebas de Mutagenicidad/métodos , Mutágenos/toxicidad , Triazinas/toxicidad , Adulto , Animales , Arocloros/farmacología , Células Cultivadas , Ensayo Cometa , Relación Dosis-Respuesta a Droga , Inducción Enzimática , Humanos , Procesamiento de Imagen Asistido por Computador , Linfocitos/efectos de los fármacos , Masculino , Pruebas de Micronúcleos , Microsomas Hepáticos/efectos de los fármacos , Microsomas Hepáticos/enzimología , Ratas , Ratas Sprague-Dawley , Intercambio de Cromátides Hermanas/efectos de los fármacosRESUMEN
Coloured polyethylene terephthalate (PET) bottles for carbonated beverages were studied for potential migration of genotoxic compounds. A combined approach, using physicochemical methods and a bacterial short-term mutagenicity test (Ames test) was followed. Standard EEC and US FDA tests for total migration of non-volatile migrant compounds into distilled water were performed, together with modified tests, where freeze-drying instead of evaporation of water was used, in order to measure both volatile and non-volatile chemicals. Gas chromatography-mass spectrometry (GC-MS) analysis was performed on these residues. PET bottles filled with naturally carbonated mineral water were also used for long-term total organic carbon (TOC) and mutagenicity migration studies (up to 6 months' storage). Total migration results for PET bottles were within the EEC and US FDA limits. The use of freeze-drying for the elimination of water enabled much higher total migration data (higher than the limits) to be revealed. Some potentially genotoxic compounds (acetaldehyde, dimethyl terephthalate, terephthalic acid) were identified in these migrant compounds by GC-MS analysis. The tests for TOC migration gave a maximum value after 2 wk storage and the mutagenicity tests on non-volatile migrant compounds gave always negative results.
Asunto(s)
Aguas Minerales , Mutágenos/análisis , Plásticos , Tereftalatos Polietilenos , Carbono/análisis , Unión Europea , Manipulación de Alimentos , Cromatografía de Gases y Espectrometría de Masas , Pruebas de Mutagenicidad , Mutágenos/toxicidad , Salmonella typhimurium/efectos de los fármacos , Solubilidad , Estados Unidos , United States Food and Drug AdministrationRESUMEN
Polyethyleneterephthalate (PET) was tested as a source of mutagen contamination from bottles used for beverage packaging. PET bottles were filled with mineral water and stored in daylight and in the dark for different periods of time. The water samples were concentrated and the concentrates (non-volatile compounds) tested for mutagenicity with the Ames test (static tests). Total organic carbon (TOC) leaching was determined concurrently. Leaching of mutagens was also studied using dynamic tests; shaking distilled water in PET bottles. New methods were also used to test the leaching potential of both volatile and non-volatile compounds: directly testing the mutagenicity in unconcentrated water stored in PET bottles and growing Salmonella strains directly in the plastic bottles. The results were positive only for the static test, which identified leaching of mutagens after 1 month of storage in PET bottles. This activity was higher after storage in daylight.
Asunto(s)
Contaminación de Alimentos/análisis , Manipulación de Alimentos , Aguas Minerales/análisis , Mutágenos/análisis , Tereftalatos Polietilenos , Pruebas de Mutagenicidad , Salmonella typhimurium/genéticaRESUMEN
During the last two decades, concerns have arisen regarding a possible association between extremely-low frequency (ELF) electromagnetic fields (EMF) exposure and cancer incidence (e.g. childhood acute leukaemia, cancer of the nervous system, and lymphomas). In 1979, Wertheimer and Leeper firstly reported an excess of cancer mortality among children living in homes located near power lines and presumably exposed to elevated magnetic fields. Subsequently, a large number of epidemiological studies investigated the possible association between residential or occupational exposure to ELF-EMF and cancer. Several in vivo and in vitro models have been investigated with the effort to determine a link, if any, between such fields and mutagenesis and to determine the possible mechanism of cancer risk. However, a causal relationship between exposure to ELF-EMF and cancer has been suggested but has not been unequivocally demonstrated. In 1998, following an analysis of the results retrieved in the literature, the U.S. National Institute of Environmental Health Sciences proposed to apply a "possible human carcinogen" category (Group 2B) to ELF-EMF. More recently, in 2002, the same classification for ELF-MF was proposed by the International Agency for Research on Cancer. In this in vitro approach, to test the genotoxic and/or co-genotoxic potency of ELF-MF, we used the alkaline single-cell microgel-electrophoresis (comet) assay and the cytokinesis block micronucleus test. Co-exposure assays were performed in the presence of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitroquinoline N-oxide (4NQO), benzene, 1,4-benzenediol (1,4-BD), or 1,2,4-benzenetriol (1,2,4-BT). An ELF-MF (50 Hz, 5 mT) was obtained by a system composed of capsulated induction coils. ELF-MF alone was unable to cause direct primary DNA damage. Whereas, an increased extent of DNA damage was observed in cells co-exposed to ELF-MF and MNNG, 1,4-BD, or 1,2,4-BT. An opposite trend was observed in cells treated with 4NQO and co-exposed to ELF-MF. Moreover, the frequency of micronucleated cells in ELF-MF-exposed cells was higher than in control cultures. Our findings suggest that the tested ELF-MF (50 Hz, 5 mT) possess genotoxic (micronucleus test) and co-genotoxic (comet assay) capabilities. The possibility that ELF-MF might interfere with the genotoxic activity of xenobiotics has important implications, since human populations are likely to be exposed to a variety of genotoxic agents concomitantly with exposure to this type of physical agent.