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Proinflammatory effects and oxidative stress within human bronchial epithelial cells exposed to atmospheric particulate matter (PM2.5 and PM>2.5) collected from Cotonou, Benin.
Environ. Pollut.
PUBLISHED: 07-04-2013
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After particulate matter (PM) collection in Cotonou (Benin), a complete physicochemical characterization of PM2.5 and PM>2.5 was led. Then, their adverse health effects were evaluated by using in vitro culture of human lung cells. BEAS-2B (bronchial epithelial cells) were intoxicated during short-term exposure at increasing PM concentrations (1.5-96 ?g/cm(2)) to determine global cytotoxicity. Hence, cells were exposed to 3 and 12 ?g/cm(2) to investigate the potential biological imbalance generated by PM toxicity. Our findings showed the ability of both PM to induce oxidative stress and to cause inflammatory cytokines/chemokines gene expression and secretion. Furthermore, PM were able to induce gene expression of enzymes involved in the xenobiotic metabolism pathway. Strong correlations between gene expression of metabolizing enzymes, proinflammatory responses and cell cycle alteration were found, as well as between proinflammatory responses and cell viability. Stress oxidant parameters were highly correlated with expression and protein secretion of inflammatory mediators.
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Xenobiotic metabolism induction and bulky DNA adducts generated by particulate matter pollution in BEAS-2B cell line: geographical and seasonal influence.
J Appl Toxicol
PUBLISHED: 06-25-2013
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Airborne particulate matter (PM) toxicity is of growing interest as diesel exhaust particles have been classified as carcinogenic to humans. However, PM is a mixture of chemicals, and respective contribution of organic and inorganic fractions to PM toxicity remains unclear. Thus, we analysed the link between chemical composition of PM samples and bulky DNA adduct formation supported by CYP1A1 and 1B1 genes induction and catalytic activities. We used six native PM samples, collected in industrial, rural or urban areas, either during the summer or winter, and carried out our experiments on the human bronchial epithelial cell line BEAS-2B. Cell exposure to PM resulted in CYP1A1 and CYP1B1 genes induction. This was followed by an increase in EROD activity, leading to bulky DNA adduct formation in exposed cells. Bulky DNA adduct intensity was associated to global EROD activity, but this activity was poorly correlated with CYPs mRNA levels. However, EROD activity was correlated with both metal and polycyclic aromatic hydrocarbon (PAH) content. Finally, principal components analysis revealed three clusters for PM chemicals, and suggested synergistic effects of metals and PAHs on bulky DNA adduct levels. This study showed the ability of PM samples from various origins to generate bulky DNA adducts in BEAS-2B cells. This formation was promoted by increased expression and activity of CYPs involved in PAHs activation into reactive metabolites. However, our data highlight that bulky DNA adduct formation is only partly explained by PM content in PAHs, and suggest that inorganic compounds, such as iron, may promote bulky DNA adduct formation by supporting CYP activity. Copyright © 2013 John Wiley & Sons, Ltd.
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Traffic-related air pollution. A pilot exposure assessment in Beirut, Lebanon.
Chemosphere
PUBLISHED: 03-12-2013
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Traffic-related volatile organic compounds (VOCs) pollution has frequently been demonstrated to be a serious problem in the developing countries. Benzene and 1,3-butadiene (BD) have been classified as a human carcinogen based on evidence for an increased genotoxic and epigenotoxic effects in both occupational exposure assessment and in vivo/in vitro studies. We have undertaken a biomonitoring of 25 traffic policemen and 23 office policemen in Beirut, through personal air monitoring, assessed by diffusive samplers, as well as through the use of biomarkers of exposure to benzene and BD. Personal benzene, toluene, ethylbenzene, and xylene (BTEX) exposure were quantified by GC-MS/MS, urinary trans, trans-muconic acid (t,t-MA) by HPLC/UV, S-phenyl mercapturic acid (S-PMA), monohydroxy-butenyl mercapturic acid (MHBMA) and dihydroxybutyl mercapturic acid (DHBMA) by ultra-performance liquid chromatography-electrospray tandem mass spectrometry (UPLC/ESI(-)-MS/MS) in MRM (Multiple Reaction Monitoring) mode. We found that individual exposure to benzene in the traffic policemen was higher than that measured in traffic policemen in Prague, in Bologna, in Ioannina and in Bangkok. t,t-MA levels could distinguish between office and traffic policemen. However, median MHBMA levels in traffic policemen were slightly elevated, though not significantly higher than in office policemen. Alternatively, DHBMA concentrations could significantly distinguish between office and traffic policemen and showed a better correlation with personal total BTEX exposure. DHMBA, measured in the post-shift urine samples, correlated with both pre-shift MHMBA and pre-shift DHMBA. Moreover, there was not a marked effect of smoking habits on DHBMA. Taken together, these findings suggested that DHBMA is more suitable than MHBMA as biomarker of exposure to BD in humans. Traffic policemen, who are exposed to benzene and BD at the roadside in central Beirut, are potentially at a higher risk for development of diseases such as cancer than office policemen.
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Polycyclic aromatic hydrocarbons within airborne particulate matter (PM(2.5)) produced DNA bulky stable adducts in a human lung cell coculture model.
J Appl Toxicol
PUBLISHED: 06-20-2011
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To extend current knowledge on the underlying mechanisms of air pollution particulate matter (PM(2.5))-induced human lung toxicity, the metabolic activation of polycyclic aromatic hydrocarbons (PAH) within PM(2.5) and PAH-DNA bulky stable adduct patterns in human alveolar macrophage (AM) and/or human lung epithelial L132 cells in mono- and cocultures were studied. In the coculture system, only human AM were exposed to air pollution PM(2.5), unlike L132 cells. Particles, inorganic fraction and positive controls [i.e. TiO(2), thermally desorbed PM (dPM) and benzo[a]pyrene, B[a]P, respectively] were included in the experimental design. Cytochrome P450 (CYP) 1A1 gene expression, CYP1A1 catalytic activity and PAH-DNA bulky stable adducts were studied after 24, 48 and/or 72 h. Relatively low doses of PAH within PM(2.5) induced CYP1A1 gene expression and CYP1A1 catalytic activity in human AM and, thereafter, PAH-DNA bulky stable adduct formation. Adduct spots in PM(2.5) -exposed human AM were higher than those in dPM-exposed ones, thereby showing the incomplete removal of PAH by thermal desorption. PAH within air pollution PM(2.5) induced CYP1A1 gene expression but not CYP1A1 catalytic activity in L132 cells. However, despite the absence of PAH-DNA bulky stable adduct in L132 cells from human AM/L132 cell cocultures exposed to dPM(2.5) or PM(2.5), reliable quantifiable PAH-DNA bulky stable adducts were observed in L132 cells from human AM/L132 cell coculture exposed to B[a]P. Taken together, these results support the exertion of genotoxicity of highly reactive B[a]P-derived metabolites produced within human AM not only in primary target human AM, but also in secondary target L132 cells.
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Assessment of fly ash-aided phytostabilisation of highly contaminated soils after an 8-year field trial Part 2. Influence on plants.
Sci. Total Environ.
PUBLISHED: 05-10-2011
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Aided phytostabilisation is a cost-efficient technique to manage metal-contaminated areas, particularly in the presence of extensive pollution. Plant establishment and survival in highly metal-contaminated soils are crucial for phytostabilisation success, as metal toxicity for plants is widely reported. A relevant phytostabilisation solution must limit metal transfer through the food chain. Therefore, this study aimed at evaluating the long-term efficiency of aided phytostabilisation on former agricultural soils highly contaminated by cadmium, lead, and zinc. The influence of afforestation and fly ash amendments on reducing metal phytoavailability was investigated as were their effects on plant development. Before being planted with a tree mix, the site was divided into three plots: a reference plot with no amendment, a plot amended with silico-aluminous fly ash and one with sulfo-calcic fly ash. Unlike Salix alba and Quercus robur, Alnus glutinosa, Acer pseudoplatanus and Robinia pseudoacacia grew well on the site and accumulated, overall, quite low concentrations of metals in their leaves and young twigs. This suggests that these three species have an excluder phenotype for Cd, Zn and Pb. After 8 years, metal availability to A. glutinosa, A. pseudoplatanus and R. pseudoacacia, and translocation to their above-ground parts, strongly decreased in fly ash-amended soils. Such decreases fit well together with the depletion of CaCl(2)-extractable metals in amended soils. Although both fly ashes were effective to decrease Cd, Pb and Zn concentrations in above-ground parts of trees, the sulfo-calcic ash was more efficient.
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Influence of fly ash aided phytostabilisation of Pb, Cd and Zn highly contaminated soils on Lolium perenne and Trifolium repens metal transfer and physiological stress.
Environ. Pollut.
PUBLISHED: 01-25-2011
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Due to anthropogenic activities, large extends of soils are highly contaminated by Metal Trace Element (MTE). Aided phytostabilisation aims to establish a vegetation cover in order to promote in situ immobilisation of trace elements by combining the use of metal-tolerant plants and inexpensive mineral or organic soil amendments. Eight years after Coal Fly Ash (CFA) soil amendment, MTE bioavailability and uptake by two plants, Lolium perenne and Trifolium repens, were evaluated, as some biological markers reflecting physiological stress. Results showed that the two plant species under study were suitable to reduce the mobility and the availability of these elements. Moreover, the plant growth was better on CFA amended MTE-contaminated soils, and the plant sensitivity to MTE-induced physiological stress, as studied through photosynthetic pigment contents and oxidative damage was lower or similar. In conclusion, these results supported the usefulness of aided phytostabilisation of MTE-highly contaminated soils.
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Assessment of fly ash-aided phytostabilisation of highly contaminated soils after an 8-year field trial: part 1. Influence on soil parameters and metal extractability.
Sci. Total Environ.
PUBLISHED: 06-28-2010
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Sustainable management of large surface areas contaminated with trace elements is a real challenge, since currently applied remediation techniques are too expensive for these areas. Aided phytostabilisation appears to be a cost efficient technique to reduce metal mobility in contaminated soils and contaminated particle spread. In this context, this study aimed at evaluating the long-term efficiency of aided phytostabilisation on former agricultural soils highly contaminated with trace elements. The influence of afforestation and fly ash amendments to reduce metal mobility was investigated. Before being planted with a tree mix, the study site was divided into three plots: a reference plot with no amendment, the second amended with silico-aluminous fly ash and the third with sulfo-calcic fly ash. After eight years, some soil physico-chemical parameters, including cadmium (Cd), lead (Pb) and zinc (Zn) extractability were modified. In particular, pH decreased on the whole site while organic carbon content increased. The alteration of these parameters influencing trace element mobility is explained by afforestation. Over time, concentrations of CaCl(2)-extractable metals increased and were correlated with the soil pH decrease. In the amended soils, extractable Cd, Pb and Zn concentrations were lower than in the reference soil. The results indicated that the two fly ashes buffered natural soil acidification due to vegetation development and limited trace element mobility and thus could limit their bioavailability. For long-term phytostabilisation, special attention should be focused on the soil pH, metal mobility and phytoavailability analysis.
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Occurrence of molecular abnormalities of cell cycle in L132 cells after in vitro short-term exposure to air pollution PM(2.5).
Chem. Biol. Interact.
PUBLISHED: 06-21-2010
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To improve the knowledge of the underlying mechanisms implying in air pollution Particulate Matter (PM)-induced lung toxicity in humans, we were interested in the sequential occurrence of molecular abnormalities from TP53-RB gene signaling pathway activation in the L132 target human lung epithelial cell model. The most toxicologically relevant physical and chemical characteristics of air pollution PM(2.5) collected in Dunkerque, a French highly-industrialized sea-side city, were determined. L132 cells were exposed during 24, 48 and 72h to Dunkerque Citys PM(2.5) (i.e. Lethal Concentration (LC)(10)=18.84?gPM/mL or 5.02?gPM/cm(2); LC(50)=75.36?gPM/mL or 20.10?gPM/cm(2)), TiO(2) and desorbed PM (i.e. dPM; EqLC(10)=15.42?g/mL or 4.11?gPM/cm(2); EqLC(50)=61.71?g/mL or 16.46?gPM/cm(2)), benzene (7?M) or Benzo[a]Pyrene (B[a]P; 1?M). Dunkerque Citys PM(2.5) altered the gene expression and/or the protein concentration of several key cell cycle controllers from TP53-RB gene signaling pathway (i.e. P53; BCL2; P21; cyclin D1, cyclin-dependent kinase 1; retinoblastoma protein) in L132 cells, thereby leading to the occurrence of cell proliferation and apoptosis together. The activation of the critical cell cycle controllers under study might be related to PM-induced oxidative stress, through the possible involvement of covalent metals in redox systems, the metabolic activation of organic chemicals by enzyme-catalyzed reactions, and phagocytosis. Taken together, these results might ask the critical question whether there is a balance or, in contrast, rather an imbalance between the cell proliferation and the apoptosis occurring in PM-exposed L132 cells, with possible consequences in term of PM-induced lung tumorgenesis.
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Seasonal and annual variations of metal uptake, bioaccumulation, and toxicity in Trifolium repens and Lolium perenne growing in a heavy metal-contaminated field.
Environ Sci Pollut Res Int
PUBLISHED: 07-08-2009
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The reclamation of nonferrous metal-polluted soil by phytoremediation requires an overall and permanent plant cover. To select the most suitable plant species, it is necessary to study metal effects on plants over the time, thereby checking that metals remain stored in root systems and not transferred to aerial parts. In this purpose, the seasonal and annual variations of metal bioaccumulation, transfer, and phytotoxicity in Trifolium repens and Lolium perenne grown in a Cd-, Pb-, and Zn-contaminated soil were also studied.
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Benzene-induced mutational pattern in the tumour suppressor gene TP53 analysed by use of a functional assay, the functional analysis of separated alleles in yeast, in human lung cells.
Arch. Toxicol.
PUBLISHED: 04-27-2009
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Recent concern has centred on the effects of continuous exposure to low concentrations of benzene, both occupationally and environmentally. Although benzene has for a long time been recognised as a carcinogen for humans, its mechanistic pathway remains unclear. Since mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancer, our objective was to establish the first mutational pattern induced by benzene on the TP53 gene in human type II-like alveolar epithelial A549 cells by using the Functional Analysis of Separated Alleles in Yeast (FASAY). Seventeen mutations linked to benzene exposure were found: 3 one- or two-base deletions, and 14 single nucleotide substitutions (1 nonsense and 13 missense mutations). A>G and G>A transitions were the most prevalent (23.5% for both). Other mutations included A>C transversions and deletions (3/17, 17.6% for both), G>T transversions (2/17, 11.8%) and A>T transversions (1/17, 5.9%). Data arising from this benzene-induced mutational pattern affecting TP53, a critical target gene in human carcinogenesis, have been compared with those reported in human acute myeloid leukaemia, the aetiology of which is clearly linked to benzene exposure, and in experimental benzene-induced carcinoma. This comparison suggests that A>G transition could be a fingerprint of benzene exposure in tumours. Furthermore, our results demonstrate that FASAY is a promising tool for the study of the carcinogenic potency of benzene in the human lung.
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Air pollution particulate matter (PM2.5)-induced gene expression of volatile organic compound and/or polycyclic aromatic hydrocarbon-metabolizing enzymes in an in vitro coculture lung model.
Toxicol In Vitro
PUBLISHED: 03-25-2009
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The overarching goals were: (i) to develop an in vitro coculture model, including two relevant lung target cells: human alveolar macrophage (AM) isolated from bronchoalveolar lavage fluid, and immortalized cells originated from the normal lung tissue of a human embryo (L132 cell line), as a future strategy for near-realistic exposures to air pollution particulate matter (PM), and (ii) to study the gene expression of volatile organic compound (VOC) and/or polycyclic aromatic hydrocarbons (PAH)-metabolizing enzymes in this in vitro coculture model. Human AM and/or L132 cells in mono- and coculture were exposed for 24, 48 and 72h to Dunkerque Citys PM2.5 at its lethal concentrations at 10% and 50% (i.e. AM: LC10=14.93 microgPM/mL and LC50=74.63 microgPM/mL; L132: LC10=18.84 microgPM/mL and LC50=75.36 microgPM/mL), and the gene expression (i.e. Cytochrome P450 1A1, CYP1A1; CYP2E1; CYP2F1; microsomal Epoxide Hydrolase; NADPH Quinone Oxydo-Reductase-1, NQO1; and Glutathione S-Transferase pi-1 and mu-3, GST-pi1 and GST-mu3) was studied. In human AM in mono- and coculture, and in L132 cells in monoculture, VOC and/or PAH-coated onto PM induced the gene expression of CYP1A1, CYP2E1, NQO1, GST-pi1, and/or GST-mu3. However, there were quiet different outcomes based on the use of L132 cells in mono- vs. coculture: the pattern of VOC and/or PAH-metabolizing enzymes induced by PM in L132 cells in monoculture remained almost unaffected when in coculture with AM. Taken together, these results reinforced the key role of PM-exposed target human AM in the defenses of the human lung from external injuries, notably through their higher capacity to retain PM, and indicated that carbonaceous cores of PM, as physical vector of the penetration and retention of coated-VOC and/or PAH into cells, enabled them to exert a longer toxicity. The use of such a near realistic exposure system could also be a very useful and powerful tool to identify the mechanisms by which air pollution PM induced adverse health effects.
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Arbuscular mycorrhiza partially protect chicory roots against oxidative stress induced by two fungicides, fenpropimorph and fenhexamid.
Mycorrhiza
PUBLISHED: 02-11-2009
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The present work examined the oxidative stress induced by different concentrations (0.02 and 0.2 mg l-1) of two sterol biosynthesis inhibitor fungicides (fenpropimorph and fenhexamid) in non-target chicory root colonised or not by Glomus intraradices in a monoxenic system. The fungicides were found to cause oxidative damage by increasing lipid peroxidation measured by malondialdehyde production in non-colonised roots. Detoxification of the H(2)O(2) product was measured at 0.2 mg l-1 of fenpropimorph by an increase in peroxidase activities suggesting an antioxidant capacity in these roots. Moreover, this study pointed out the ability of arbuscular mycorrhiza to alleviate partially the oxidative stress in chicory roots, probably by lowering reactive oxygen species concentrations, resulting from increases in antioxidant defences. Our results suggest that the enhanced fungicide tolerance in the AM symbiosis could be related to less cell membrane damage.
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Role of air pollution Particulate Matter (PM(2.5)) in the occurrence of loss of heterozygosity in multiple critical regions of 3p chromosome in human epithelial lung cells (L132).
Toxicol. Lett.
PUBLISHED: 01-26-2009
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Lung cancer still remains the most frequent type of cancer all around the world and the leading cause of cancer-related death. Even if tobacco use takes a major part in etiology of lung cancer, other explanations like genetic and lifestyle factors, and occupational and/or environmental exposure to carcinogens have to be considered. Hence, in this study, we were interested in the ability of in vitro short-term exposure to air pollution Particulate Matter (PM) to induce genomic alterations in Dunkerque Citys PM(2.5)-exposed human epithelial lung cells (L132). The occurrence of MicroSatellite (MS) alterations in 3p multiple critical regions (i.e. 3p14.1, 3p14.2, 3p14.3, 3p21.1, 3p21.31, and 3p21.32) identified as showing frequent allelic losses in benign or malignant lung diseases, was also studied in Dunkerque Citys PM(2.5)-exposed L132 cells. Negative (i.e. TiO(2); desorbed PM, dPM), and positive (i.e. benzo[a]pyrene, B[a]P) controls were also included in the experimental design. Loss Of Heterozygosity (LOH) and/or MicroSatellite Instability (MSI) were reported 72h after L132 cell exposure to dPM (i.e. 61.71microg dPM/mL or 12.34microgdPM/cm(2)), PM (i.e. 75.36microgPM/mL or 15.07microgPM/cm(2)), or B[a]P (i.e. 1microM). In agreement with the current literature, such MS alterations might rely on the ability of dPM, PM or B[a]P to induce oxidative stress conditions, thereby altering DNA polymerase enzymes, enhancing DNA recombination rates, and inhibiting DNA repair enzymes. Hence, we concluded that the occurrence of dramatic MS alterations in 3p chromosome multiple critical regions could be a crucial underlying mechanism, which proceeded the lung toxicity in air pollution PM-exposed target L132 cells.
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Mycorrhization alleviates benzo[a]pyrene-induced oxidative stress in an in vitro chicory root model.
Phytochemistry
PUBLISHED: 01-23-2009
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Among chemicals that are widely spread both in terrestrial and aquatic ecosystems, benzo[a]pyrene is a major source of concern. However, little is known about its adverse effects on plants, as well as about the role of mycorrhization in protection of plant grown in benzo[a]pyrene-polluted conditions. Hence, to contribute to a better understanding of the adverse effects of polycyclic aromatic hydrocarbons on the partners of mycorrhizal symbiotic association, benzo[a]pyrene-induced oxidative stress was studied in transformed Cichorium intybus roots grown in vitro and colonized or not by Glomus intraradices. The arbuscular mycorrhizal fungus development (colonization, extraradical hyphae length, and spore formation) was significantly reduced in response to increasing concentrations of benzo[a]pyrene (35-280 microM). The higher length of arbuscular mycorrhizal roots, compared to non-arbuscular mycorrhizal roots following benzo[a]pyrene exposure, pointed out a lower toxicity of benzo[a]pyrene in arbuscular mycorrhizal roots, thereby suggesting protection of the roots by mycorrhization. Accordingly, in benzo[a]pyrene-exposed arbuscular mycorrhizal roots, statistically significant decreases were observed in malondialdehyde concentration and 8-hydroxy-2-desoxyguanosine formation. The higher superoxide dismutase activity detected in mycorrhizal chicory roots could explain the benzo[a]pyrene tolerance of the colonized roots. Taken together, these results support an essential role of mycorrhizal fungi in protecting plants submitted to polycyclic aromatic hydrocarbon, notably by reducing polycyclic aromatic hydrocarbon-induced oxidative stress damage.
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Xenobiotic metabolism and disposition in human lung cell models: comparison with in vivo expression profiles.
Drug Metab. Dispos.
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Numerous lung cell lines are currently used as in vitro models for pharmacological and toxicological studies. However, no exhaustive report about the metabolic capacities of these models in comparison with those of lung tissues is available. In the present study, we used a high-throughput quantitative real-time reverse transcription-polymerase chain reaction strategy to characterize the expression profiles of 380 genes encoding proteins involved in the metabolism and disposition of xenobiotics in 10 commonly used lung cell lines (A549, H292, H358, H460, H727, Calu-1, 16HBE, 1 HAEO, BEAS-2B, and L-132) and four primary cultures of human bronchial epithelial cells. Expression results were then compared with those previously obtained in human nontumoral and tumoral lung tissues. Our results revealed disparities in gene expression between lung cell lines or when comparing lung cell lines with primary cells or lung tissues. Primary cell cultures displayed the highest similarities with bronchial mucosa in terms of transcript profiling and therefore seem to be the most relevant in vitro model for investigating the metabolism and bioactivation of toxicants and drugs in bronchial epithelium. H292 and BEAS-2B cell lines, which exhibited the highest homology in gene expression pattern with primary cells and the lowest number of dysregulated genes compared with nontumoral lung tissues, could be used as surrogates for toxicological and pharmacological studies. Overall, our study should provide references for researchers to choose the most appropriate in vitro model for analyzing the cellular effects of drugs or airborne toxicants on the airway.
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Prooxidant and proinflammatory potency of air pollution particulate matter (PM?.???.?) produced in rural, urban, or industrial surroundings in human bronchial epithelial cells (BEAS-2B).
Chem. Res. Toxicol.
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Compelling evidence indicates that exposure to air pollution particulate matter (PM) affects human health. However, how PM composition interacts with PM-size to cause adverse health effects needs elucidation. In this study, we were also interested in the physicochemical characteristics and toxicological end points of PM?.???.? samples produced in rural, urban, or industrial surroundings, thereby expecting to differentiate their respective in vitro adverse health effects in human bronchial epithelial cells (BEAS-2B). Physicochemical characteristics of the three PM?.???.? samples, notably their inorganic and organic components, were closely related to their respective emission sources. Referring also to the dose/response relationships of the three PM?.???.? samples, the most toxicologically relevant exposure times (i.e., 24, 48, and 72 h) and doses (i.e., 3.75 ?g PM/cm² and 15 ?g PM/cm²) to use to study the underlying mechanisms of action involved in PM-induced lung toxicity were chosen. Organic chemicals adsorbed on the three PM?.???.? samples (i.e., polycyclic aromatic hydrocarbons) were able to induce the gene expression of xenobiotic-metabolizing enzymes (i.e., Cytochrome P4501A1 and 1B1, and, to a lesser extent, NADPH-quinone oxidoreductase-1). Moreover, intracellular reactive oxygen species within BEAS-2B cells exposed to the three PM?.???.? samples induced oxidative damage (i.e., 8-hydroxy-2-deoxyguanosine formation, malondialdehyde production and/or glutathione status alteration). There were also statistically significant increases of the gene expression and/or protein secretion of inflammatory mediators (i.e., notably IL-6 and IL-8) in BEAS-2B cells after their exposure to the three PM?.???.? samples. Taken together, the present findings indicated that oxidative damage and inflammatory response preceeded cytotoxicity in air pollution PM?.???.?-exposed BEAS-2B cells and supported the idea that PM-size, composition, and origin could interact in a complex manner to determine the in vitro responsiveness to PM.
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Benzo[a]pyrene, aflatoxine B? and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology.
PLoS ONE
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Mutations in the TP53 gene are the most common alterations in human tumours. TP53 mutational patterns have sometimes been linked to carcinogen exposure. In hepatocellular carcinoma, a specific G>T transversion on codon 249 is classically described as a fingerprint of aflatoxin B(1) exposure. Likewise G>T transversions in codons 157 and 158 have been related to tobacco exposure in human lung cancers. However, controversies remain about the interpretation of TP53 mutational pattern in tumours as the fingerprint of genotoxin exposure. By using a functional assay, the Functional Analysis of Separated Alleles in Yeast (FASAY), the present study depicts the mutational pattern of TP53 in normal human fibroblasts after in vitro exposure to well-known carcinogens: benzo[a]pyrene, aflatoxin B(1) and acetaldehyde. These in vitro patterns of mutations were then compared to those found in human tumours by using the IARC database of TP53 mutations. The results show that the TP53 mutational patterns found in human tumours can be only partly ascribed to genotoxin exposure. A complex interplay between the functional impact of the mutations on p53 phenotype and the cancer natural history may affect these patterns. However, our results strongly support that genotoxins exposure plays a major role in the aetiology of the considered cancers.
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Relationship between physicochemical characterization and toxicity of fine particulate matter (PM2.5) collected in Dakar city (Senegal).
Environ. Res.
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The massive increase in emissions of air pollutants due to economic and industrial growth in developing countries has made air quality a crucial health problem in this continent. Hence, it is somewhat critical to have a better knowledge on the air pollution in Sub-Saharan Africa countries. Three air pollution PM2.5 samples were also collected in two urban sites (i.e., Fann and Faidherbe) in Dakar (Senegal) and in a rural site near Dakar (i.e., Ngaparu). The two urban sites mainly differ in the type of used vehicles: in Fann, most of the traffic is made of buses, which are absent, in Faidherbe. The physicochemical characteristics of the three PM2.5 samples revealed their high heterogeneities and complexities, related to the multiple natural and anthropogenic emission sources. Results from 5-bromodeoxyuridine incorporation into DNA, mitochondrial dehydrogenase activity, and extracellular lactate dehydrogenase activity in PM2.5-exposed BEAS-2B cells suggested the exposure conditions (i.e., 3 and 12 ?g PM/cm² during 24, 48, and 72 h) to further consider. The organic fractions (i.e., mainly PAHs) of the PM(2.5) samples were able to induce a time and/or concentration-dependent gene expression of CYP1A1 and CYP1B1, and, to a lesser extent, NQO1. There was a time and/or dose-dependent increase of both the gene expression and/or protein secretion of inflammatory mediators (i.e., TNF-?, IL-1?, IL-6, and/or IL-8) in PM(2.5)-exposed BEAS-2B cells. In agreement with the physicochemical characterization, urban PM(2.5) samples caused greater biological responses in BEAS-2B cells than the rural one. Variable concentrations of transition metals (i.e., Fe, Al, Pb, Mn, Zn) and organic compounds (i.e., PAHs) founded in the three PM2.5 samples might be firmly involved in a time- and/or dose-dependent toxicity, relying on inflammatory processes.
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