1,721,014 research outputs found
Determination of anti-BPDE-DNA adducts in pah-exposed humans using the HPLC/fluorescence technique
No full textIn the present study, HPLC/fluorescence was applied to determine anti (±)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adducts formed in lymphocytes plus monocytes (LMF) from humans exposed to polycyclic aromatic hydrocarbons (PAH). Subjects were: 10 psoriatic patients (3 days after clinical coal tar (CT) treatment), 15 coke oven workers, 19 chimney sweeps, 35 aluminum anode plant workers, and 10 control subjects. Chronic and high PAH exposure in coke oven workers significantly increased the levels of BPDE-DNA adducts and the highest levels were seen in samples from smokers. Skin-acute (or short-term) and high PAH exposure of psoriatic patients do not increase DNA adduct levels. Determination of anti-BPDE-DNA adducts by means of this method is very promising for its sensitivity, specificity and simplicity and it may be applied in DNA adduct measurements to assesss high chronic PAH exposure and that it is thus suitable for industrial health purposes
[CYP1A2, NAT2, and GSTM1 phenotype/genotype modulate human exposure and various environmental mutagens: our experience]
No full textSince some years in our research group has been studied the influence of metabolic genotypes on two biomarkers of genotoxic risk (BPDE-DNA adducts and urinary mutagenicity) in humans exposed to polycyclic aromatic hydrocarbons (PAHs) and aromatic amines. The aim was to identify possible genetic susceptible factors capable of modulating individual response to these carcinogens. Humans exposed to PAHs: dermatological patients therapeutically treated with coal tar based ointments (CT), coke oven workers and chimney sweeps. People exposed to aromatic amines will be volunteers after a meal of pan-fried hamburgers and smokers. An overview of the results we found until now will be presented
Valori di riferimento nel monitoraggio biologico dell'esposizione professionale ad agenti mutageni e cancerogeni
No full text[Reference values in biological monitoring of occupational exposure to mutagens and carcinogens]
No full textThis work reports values of biological markers indicating mutagenic/carcinogenic risk in professionally non-exposed populations. The main confounding factors for most of these biomarkers are tobacco smoke, diet and air pollution. With the sole exception of compounds specifically present in work environments, in which determination in biological fluids of unchanged substances or their metabolites has high sensitivity and specificity (e.g., some aromatic amines), other biomarkers (urinary mutagenicity, DNA adducts and cytogenetic analyses), in order to be used properly as reference values, require ad hoc study of suitable control groups paired for the main confounding factors. Analytical determination of some protein adducts appears to be promising, due to its sensitivity and specificity
Indicatori di dose biologicamente efficace
No full textBiologically effective dose markers –DNA and protein adducts- are classified among the exposure biomarkers, and nowadays they are used to assess the biologically active fraction of xenobiotics, able to interact with cellular macromolecules at the target site.
Actually, macromolecular adducts can be considered not only as exposure indicators, but their biological significance can be extended also to biomarkers of effect and of susceptibility. The achievement of such a goal need research programs aimed both to study molecular mechanisms related to each steps along the continuum of events between exposure and disease, and to establish quantitative relationships between exposure levels and adducts formation, between adducts and early biological effects, effects and cellular structural/functional modifications, till the development and eventually the incidence increment of specific pathologies. Besides, different factors must be considered during data evaluation, such as: the interindividual variability, the background levels of biomarkers in non occupationally exposed population, the lower and lower doses of genotoxic agents involved in occupational exposures, confounding factors such as diet and smoking habits.
Despite the large body of literature documenting DNA and protein adduct molecular dosimetry for many carcinogen exposures, many authors claimed the necessity of systematic interlaboratory comparisons and collaborations by measuring the same biomarkers with different techniques and/or different biomarkers related to the same exposure levels. There is also a general agreement in the need of validated and standardized analytical procedures without neglecting analytical times and costs, so that dosimetric analyses could be economically advantageous and accessible in all cases they prove to be useful in preventing health risks
Influence of the genetic polymorphism in the 5'-noncoding region of the CYP1A2 gene on CYP1A2 phenotype and urinary mutagenicity in smokers
No full textThe functional significance of genetic polymorphisms on tobacco smoke-induced CYP1A2 activity was examined. The influence of three polymorphisms of the cytochrome P450 1A2 gene (CYP1A2) (-3860 G-->A (allele *1C), -2467 T-->delT (allele *1D), -163C-->A (allele *1F)), located in the 5'-noncoding promoter region of the gene, on CYP1A2 activity (measured as caffeine metabolic ratio, CMR), was studied in Caucasian current smokers (n=95). Tobacco smoke intake was calculated from the number of cigarettes/day. Also, studied was the influence of these CYP1A2 genotypes on smoking-associated urinary mutagenicity, detected in Salmonella typhimurium strain YG1024 with S9 mix, considering the urinary excretion of nicotine plus its metabolites as an internal indicator of tobacco smoke exposure. Smokers with at least one of the variant alleles CYP1A2 -3860A and -2467 delT showed a significantly increased CYP1A2 CMR (-3860 G/A versus G/G, por=0.69 mg/mmol creatinine) with variant allele -2467delT or -163A had significantly increased urinary mutagenicity (pdelT having the main effect. This information is of interest for future studies assessing the possible role of tobacco smoke-inducible CYP1A2 genotypes as individual susceptibility factors in exposure to carcinogens
Misura del LAeq del rumore impulsivo: confronto tra vari tipi di dosimetri
No full textData l'estrema tentazione, per chi opera nel campo dell'Igiene Industriale, di usare strumenti come i dosimetri di rumore che hanno dei requisiti ottimali visto il loro basso costo e la loro indossabilità da parte del lavoratore per tutta una giornata lavorativa, permettendo in conclusione di risolvere semplicemente il problema della valutazione del rischio, la ricerca sperimentale ha voluto verificare se alcuni dosimetri, attualmente presenti sul mercato italiano, possiedono sufficienti caratteristiche per fornire un attendibile Laeq in presenza di rumori impulsivi. Infatti solo in caso di risposta affermativa è presumibile individuare dal Laeq del dosimetro il rischio di sordità professionale basato sul Principio di Uguale Quantità di Energia
Non smoking coke oven workers have urinary mutagenicity levels related to occupational PAH exposure
No full textMutagenic Activity of Overnight Urine from Healthy Non-Smoking Subjects
No full textUrinary mutagenicity was evaluated in relation to environmental mutagen exposure (i.e., diet, indoor/outdoor activities, residential area etc.) on the day prior to sample collection, and also considering factors that contribute to the variability of Salmonella mutagenicity assay results. Overnight urine samples from 283 healthy non-smoking residents of northeast Italy (46% males, 20-62 years) were analyzed for mutagenicity on sensitive Salmonella typhimurium strain YG1024 with S9 mix employing the preincubation version of the plate incorporation assay (i.e., the Salmonella reverse mutation test). Urinary mutagenicity varied between 0.02 and 9.84 rev/ equiv. ml, and 7% of samples were positive (i.e., sample elicited a two-fold increase in revertants). There was an evident increase in mutagenicity in subjects with increased intake of mutagen-rich meals (n = 80) (P < 0.01 and positive urine 13% vs. 5%, P = 0.025). Indoor-exposed subjects (n = 65) also showed a higher percentage of positive urine (14% vs. 5%, P = 0.015). In particular, those subjects exposed to cooking fumes the previous evening (n = 28) revealed higher urinary mutagenicity (P = 0.035, positive urine 25% vs. 5%, P < 0.001) than non-indoor exposed. The sources of variability of the mutagenicity assay, mainly the histidine content of the urine concentrate (z = 4.06, P < 0.0001), and to a lesser extent bacterial inoculum size (z = 2.33, P = 0.019), also significantly influenced urinary mutagenicity values. In a linear multiple regression analysis, their effects were still significant (i.e., histidine content P = 0.026 and inoculum size P = 0.021), but the effects of diet, indoor exposure, and other environmental exposures (i.e., traffic and heating system exhausts, residential area) were not. It is concluded that the previous day's exposure to mutagen-rich meals and cooking fumes may influence the presence of mutagenic activity in the overnight urine of non-smoking subjects. This mutagenic activity, which remains in contact with bladder mucosa for several hours, could be considered risk factors for colorectal adenoma and possibly other cancers (i.e., bladder) in non-smokers. Accurate control of histidine content and bacterial inoculum size is strongly recommended when investigating the mutagenic activity of urine from non-smokers. (c) 2007 Wiley-Liss, Inc.
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