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202 results on '"Garçon, G."'

4. OS01-02: Impact of heated tobacco product, electronic cigarette and conventional cigarette emissions on the generation of oxidative stress, genetic and epigenetic lesions in human bronchial epithelial cells

Author

Zarcone, G., primary, Lenski, M., additional, Martinez, T., additional, Talahari, S., additional, Simonin, O., additional, Garçon, G., additional, Allorge, D., additional, Nesslany, F., additional, Lo Guidice, J.-M., additional, Platel, A., additional, and Antherieu, S., additional

Published
2023
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11. Trial of Deferiprone in Parkinson's Disease

Author

Devos, D., Labreuche, J., Rascol, O., Corvol, J.C., Duhamel, A., Delannoy, P. Guyon, Poewe, W., Compta, Y., Pavese, N., Růžička, E., Dušek, P., Post, B., Bloem, B.R., Berg, D., Maetzler, W., Otto, M., Habert, M.O., Lehericy, S., Ferreira, J., Dodel, R., Tranchant, C., Eusebio, A., Thobois, S., Marques, A.R., Meissner, W.G., Ory-Magne, F., Walter, U., Bie, R.M. de, Gago, M., Vilas, D., Kulisevsky, J., Januario, C., Coelho, M.V.S., Behnke, S., Worth, P., Seppi, K., Ouk, T., Potey, C., Leclercq, C., Viard, R., Kuchcinski, G., Lopes, R., Pruvo, J.P., Pigny, P., Garçon, G., Simonin, O., Carpentier, J., Rolland, A.S., Nyholm, D., Scherfler, C., Mangin, J.F., Chupin, M., Bordet, R., Dexter, D.T., Fradette, C., Spino, M., Tricta, F., Ayton, S., Bush, A.I., Devedjian, J.C., Duce, J.A., Cabantchik, I., Defebvre, L., Deplanque, D., Moreau, C., Devos, D., Labreuche, J., Rascol, O., Corvol, J.C., Duhamel, A., Delannoy, P. Guyon, Poewe, W., Compta, Y., Pavese, N., Růžička, E., Dušek, P., Post, B., Bloem, B.R., Berg, D., Maetzler, W., Otto, M., Habert, M.O., Lehericy, S., Ferreira, J., Dodel, R., Tranchant, C., Eusebio, A., Thobois, S., Marques, A.R., Meissner, W.G., Ory-Magne, F., Walter, U., Bie, R.M. de, Gago, M., Vilas, D., Kulisevsky, J., Januario, C., Coelho, M.V.S., Behnke, S., Worth, P., Seppi, K., Ouk, T., Potey, C., Leclercq, C., Viard, R., Kuchcinski, G., Lopes, R., Pruvo, J.P., Pigny, P., Garçon, G., Simonin, O., Carpentier, J., Rolland, A.S., Nyholm, D., Scherfler, C., Mangin, J.F., Chupin, M., Bordet, R., Dexter, D.T., Fradette, C., Spino, M., Tricta, F., Ayton, S., Bush, A.I., Devedjian, J.C., Duce, J.A., Cabantchik, I., Defebvre, L., Deplanque, D., and Moreau, C.

Abstract

Item does not contain fulltext, BACKGROUND: Iron content is increased in the substantia nigra of persons with Parkinson's disease and may contribute to the pathophysiology of the disorder. Early research suggests that the iron chelator deferiprone can reduce nigrostriatal iron content in persons with Parkinson's disease, but its effects on disease progression are unclear. METHODS: We conducted a multicenter, phase 2, randomized, double-blind trial involving participants with newly diagnosed Parkinson's disease who had never received levodopa. Participants were assigned (in a 1:1 ratio) to receive oral deferiprone at a dose of 15 mg per kilogram of body weight twice daily or matched placebo for 36 weeks. Dopaminergic therapy was withheld unless deemed necessary for symptom control. The primary outcome was the change in the total score on the Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS; range, 0 to 260, with higher scores indicating more severe impairment) at 36 weeks. Secondary and exploratory clinical outcomes at up to 40 weeks included measures of motor and nonmotor disability. Brain iron content measured with the use of magnetic resonance imaging was also an exploratory outcome. RESULTS: A total of 372 participants were enrolled; 186 were assigned to receive deferiprone and 186 to receive placebo. Progression of symptoms led to the initiation of dopaminergic therapy in 22.0% of the participants in the deferiprone group and 2.7% of those in the placebo group. The mean MDS-UPDRS total score at baseline was 34.3 in the deferiprone group and 33.2 in the placebo group and increased (worsened) by 15.6 points and 6.3 points, respectively (difference, 9.3 points; 95% confidence interval, 6.3 to 12.2; P<0.001). Nigrostriatal iron content decreased more in the deferiprone group than in the placebo group. The main serious adverse events with deferiprone were agranulocytosis in 2 participants and neutropenia in 3 participants. CONCLUSIONS: In parti

Published
2022

14. Metal enriched quasi-ultrafine particles from gas metal arc welding-stainless steel induced genetic and epigenetic alterations in BEAS-2B cells

Author

Boudjema, J., primary, Lima, B., additional, Grare, C., additional, Alleman, L.Y., additional, Rousset, D., additional, Perdrix, E., additional, Achour, D., additional, Anthérieu, S., additional, Platel, A., additional, Nesslany, F., additional, Leroyer, A., additional, Nisse, C., additional, Lo Guidice, J.M., additional, and Garçon, G., additional

Published
2021
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17. Long-term respiratory impact of electronic cigarette

Author

Dusautoir, R., primary, Zarcone, G., additional, Platel, A., additional, Kervoaze, G., additional, Laine, W., additional, Kluza, J, additional, Nesslany, F., additional, Gosset, P., additional, Garçon, G., additional, Anthérieu, S., additional, and Lo Guidice, J.-M., additional

Published
2021
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18. Metal enriched quasi-ultrafine particles from stainless steel gas metal arc welding induced genetic and epigenetic alterations in BEAS-2B cells

Author

Boudjema, J., primary, Lima, B., additional, Grare, C., additional, Alleman, L.Y., additional, Rousset, D., additional, Perdrix, E., additional, Achour, D., additional, Anthérieu, S., additional, Platel, A., additional, Nesslany, F., additional, Leroyer, A., additional, Nisse, C., additional, Lo Guidice, J.-M., additional, and Garçon, G., additional

Published
2021
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19. Modifying effect of ceruloplasmin polymorphism on iron chelation response in Parkinsonʼs disease: 652

Author

Grolez, G., Meguig, S., Moreau, C., Sablonnière, B., Strubi-Vuilhaume, I., Ryckewaert, G., Jissendi, P., Hopes, L., Dujardin, K., Devedjian, J.-C., Kluza, J., Laloux, C., Jonneaux, A., Petrault, M., Garçon, G., Rouaix, N., Duhamel, A., Auger, F., Ravasi, L., Firdaus, W., Zahr, N., Destée, A., Corvol, J.-C., Pöltl, D., Leist, M., Rose, C., Marchetti, P., Cabantchik, I. Z., Bordet, R., Defebvre, L., and Devos, D.

Published
2014

21. Mitochondrial alterations triggered by repeated exposure to fine (PM2.5-0.18) and quasi-ultrafine (PM0.18) fractions of ambient particulate matter

Author

Sotty, J., Kluza, J., de Sousa, C., Tardivel, M., Antherieu, S., Alleman, L.-Y., Canivet, L., Perdrix, E., Loyens, A., Marchetti, P., Lo Guidice, J.-M., Garçon, G., Impact de l'environnement chimique sur la santé humaine - ULR 4483 (IMPECS), Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Plate-forme d'imagerie cellulaire BICEL-IFR 114, Pôle Recherche, University of Lille, Lille, Centre for Energy and Environment (CERI EE), Ecole nationale supérieure Mines-Télécom Lille Douai (IMT Lille Douai), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT), Institut Mines-Télécom [Paris] (IMT), Lille Neurosciences & Cognition - U 1172 (LilNCog (ex-JPARC)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), CCSD, Accord Elsevier, Plateforme BioImaging Center Lille (BICeL), Plateformes Lilloises en Biologie et Santé - UAR 2014 - US 41 (PLBS), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur de Lille, Centre for Energy and Environment (CERI EE - IMT Nord Europe), Ecole nationale supérieure Mines-Télécom Lille Douai (IMT Nord Europe), and Lille Neurosciences & Cognition - U 1172 (LilNCog)

Subjects
lcsh:GE1-350, [SDE] Environmental Sciences, Fine particles, Quasi-ultrafine particles, Toxicity, [SDE]Environmental Sciences, Normal human bronchial epithelial BEAS-2B cells, Mitochondrial dynamics, Mitochondrial function, lcsh:Environmental sciences, ComputingMilieux_MISCELLANEOUS
Abstract

Nowadays ambient particulate matter (PM) levels still regularly exceed the guideline values established by World Health Organization in most urban areas. Numerous experimental studies have already demonstrated the airway toxicity of the fine fraction of PM (FP), mainly triggered by oxidative stress-induced airway inflammation. However, only few studies have actually paid close attention to the ultrafine fraction of PM (UFP), which is likely to be more easily internalized in cells and more biologically reactive. Mitochondria are major endogenous sources of reactive oxygen species (ROS) through oxidative metabolism, and coordinate many critical cellular signaling processes. Mitochondria have been often studied in the context of PM toxicity and generally associated with apoptosis activation. However, little is known about the underlying adaptation mechanisms that could occur following exposure at sub-apoptotic doses of ambient PM. Here, normal human bronchial epithelial BEAS-2B cells were acutely or repeatedly exposed to relatively low doses (5 µg.cm−2) of FP (PM2.5-0.18) or quasi-UFP (Q-UFP; PM0.18) to better access the critical changes in mitochondrial morphology, functions, and dynamics. No significant cytotoxicity nor increase of apoptotic events were reported for any exposure. Mitochondrial membrane potential (ΔΨm) and intracellular ATP content were also not significantly impaired. After cell exposure to sub-apoptotic doses of FP and notably Q-UFP, oxidative phosphorylation was increased as well as mitochondrial mass, resulting in increased production of mitochondrial superoxide anion. Given this oxidative boost, the NRF2-ARE signaling pathway was significantly activated. However, mitochondrial dynamic alterations in favor of accentuated fission process were observed, in particular after Q-UFP vs FP, and repeated vs acute exposure. Taken together, these results supported mitochondrial quality control and metabolism dysfunction as an early lung underlying mechanism of toxicity, thereby leading to accumulation of defective mitochondria and enhanced endogenous ROS generation. Therefore, these features might play a key role in maintaining PM-induced oxidative stress and inflammation within lung cells, which could dramatically contribute to the exacerbation of inflammatory chronic lung diseases. The prospective findings of this work could also offer new insights into the physiopathology of lung toxicity, arguably initiate and/or exacerbate by acutely and rather repeated exposure to ambient FP and mostly Q-UFP.

Published
2020

22. Study of in vitro and in vivo genotoxic effects of air pollution fine (PM2.5-0.18) and quasi-ultrafine (PM0.18) particles on lung models

Author

Platel, A., primary, Privat, K., additional, Talahari, S., additional, Delobel, A., additional, Dourdin, G., additional, Gateau, E., additional, Simar, S., additional, Saleh, Y., additional, Sotty, J., additional, Antherieu, S., additional, Canivet, L., additional, Alleman, L.-Y., additional, Perdrix, E., additional, Garçon, G., additional, Denayer, F.O., additional, Lo Guidice, J.M., additional, and Nesslany, F., additional

Published
2020
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24. A ferroptosis-based panel of prognostic biomarkers for Amyotrophic Lateral Sclerosis.

Author

Devos, D, Moreau, C, Kyheng, M, Garçon, G, Rolland, AS, Blasco, H, Gelé, P, Timothée Lenglet, T, Veyrat-Durebex, C, Corcia, P, Dutheil, M, Bede, P, Jeromin, A, Oeckl, P, Otto, M, Meininger, V, Danel-Brunaud, V, Devedjian, J-C, Duce, JA, Pradat, PF, Devos, D, Moreau, C, Kyheng, M, Garçon, G, Rolland, AS, Blasco, H, Gelé, P, Timothée Lenglet, T, Veyrat-Durebex, C, Corcia, P, Dutheil, M, Bede, P, Jeromin, A, Oeckl, P, Otto, M, Meininger, V, Danel-Brunaud, V, Devedjian, J-C, Duce, JA, and Pradat, PF

Abstract

Accurate patient stratification into prognostic categories and targeting Amyotrophic Lateral Sclerosis (ALS)-associated pathways may pave the way for promising trials. We evaluated blood-based prognostic indicators using an array of pathological markers. Plasma samples were collected as part of a large, phase III clinical trial (Mitotarget/TRO19622) at months 1, 6, 12 and 18. The ALSFRS-r score was used as a proxy of disease progression to assess the predictive value of candidate biological indicators. First, established clinical predictors were evaluated in all 512 patients. Subsequently, pathologic markers, such as proxies of neuronal integrity (Neurofilament light chain and phosphorylated heavy chain), DNA oxidation (8-oxo-2'-desoxyguanosine), lipid peroxidation (4-hydroxy-2-nonenal, isoprostane), inflammation (interleukin-6) and iron status (ferritin, hepcidin, transferrin) were assessed in a subset of 109 patients that represented the whole cohort. Markers of neuronal integrity, DNA and lipid oxidation, as well as iron status at baseline are accurate predictors of disability at 18-month follow-up. The composite scores of these markers in association with established clinical predictors enable the accurate forecasting of functional decline. The identified four biomarkers are all closely associated with 'ferroptosis', a recently discovered form of programmed cell death with promising therapeutic targets. The predictive potential of these pathophysiology-based indicators may offer superior patient stratification for future trials, individualised patient care and resource allocation.

Published
2019

25. Could Conservative Iron Chelation Lead to Neuroprotection in Amyotrophic Lateral Sclerosis?

Author

Moreau, C, Danel, V, Devedjian, JC, Grolez, G, Timmerman, K, Laloux, C, Petrault, M, Gouel, F, Jonneaux, A, Dutheil, M, Lachaud, C, Lopes, R, Kuchinski, G, Auger, F, Kyheng, M, Duhamel, A, Pérez, T, Pradat, P-F, Blasco, H, Veyrat-Durebex, C, Corcia, P, Oeckl, P, Otto, M, Dupuis, L, Garçon, G, Defebvre, L, Cabantchik, IZ, Duce, J, Bordet, R, Devos, D, Sexualité et soins (Genre, Sexualité, Santé) (CESP - INSERM U1018 - Equipe 7), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), Johns Hopkins Bloomberg School of Public Health [Baltimore], Johns Hopkins University (JHU), Troubles cognitifs dégénératifs et vasculaires - U 1171 (TCDV), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Evaluation des technologies de santé et des pratiques médicales - ULR 2694 (METRICS), Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institut méditerranéen de biodiversité et d'écologie marine et continentale (IMBE), Avignon Université (AU)-Aix Marseille Université (AMU)-Institut de recherche pour le développement [IRD] : UMR237-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Francois Rabelais [Tours], Imagerie et cerveau (iBrain - Inserm U1253 - UNIV Tours ), Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Biochimie [CHRU Tours], Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Universität Ulm - Ulm University [Ulm, Allemagne], Laboratoire de signalisation moléculaire et neurodégénerescence, Université Louis Pasteur - Strasbourg I-IFR37-Institut National de la Santé et de la Recherche Médicale (INSERM), Impact de l'environnement chimique sur la santé humaine - ULR 4483 (IMPECS), Service de neurologie et pathologie du mouvement, Hôpital Roger Salengro [Lille]-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), The Florey Institute of Neuroscience and Mental Health, University of Melbourne, University of Leeds, Troubles cognitifs dégénératifs et vasculaires - U 1171 - EA 1046 (TCDV), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Tours-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Régional Universitaire de Tours (CHRU TOURS), CHU Lille, CNRS, Inserm, Institut Pasteur de Lille, Université de Lille, Troubles cognitifs dégénératifs et vasculaires - U1171, Physiologie Cellulaire (PHYCEL) - U1003, METRICS : Evaluation des technologies de santé et des pratiques médicales - ULR 2694, IMPact de l'Environnement Chimique sur la Santé humaine (IMPECS) - ULR 4483, Santé publique : épidémiologie et qualité des soins - EA 2694, Centre d'Infection et d'Immunité de Lille (CIIL) - U1019 - UMR 8204, IMPact de l'Environnement Chimique sur la Santé humaine (IMPECS) - EA 4483, Lille Neurosciences & Cognition (LilNCog) - U 1172, 425779|||Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille], Thérapies Lasers Assistées par l'Image pour l'Oncologie (ONCO-THAI) - U1189, Troubles cognitifs dégénératifs et vasculaires - U 1171 [TCDV], Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille], Evaluation des technologies de santé et des pratiques médicales - ULR 2694 [METRICS], Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL], CHU Pitié-Salpêtrière [AP-HP], Centre Hospitalier Régional Universitaire de Tours [CHRU Tours], Université de Strasbourg [UNISTRA], Impact de l'environnement chimique sur la santé humaine - ULR 4483 [IMPECS], The Hebrew University of Jerusalem [HUJ], University of Cambridge [UK] [CAM], Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille, Centre National de la Recherche Scientifique (CNRS)-Institut de recherche pour le développement [IRD] : UMR237-Aix Marseille Université (AMU)-Avignon Université (AU), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université d'Angers (UA), Département de neurologie [Lille], Département de Pharmacologie Médicale [Lille] [Pôle Recherche], 451074|||Troubles cognitifs dégénératifs et vasculaires - U 1171 [TCDV], Service de Biostatistiques [CHRU Lille], Laboratoire d'Imagerie Biomédicale [Paris] [LIB], Laboratoire de Biochimie et de Biologie Moléculaire, and Laboratoire de Biochimie Médicale et Biologie Moléculaire

Subjects
Adult, Male, amyotrophic lateral sclerosis, oxidative stress, neuroprotection, treatment, conservative iron chelator, Dose-Response Relationship, Drug, [SDV]Life Sciences [q-bio], Mice, Transgenic, Middle Aged, Iron Chelating Agents, Neuroprotection, Disease Models, Animal, Mice, Young Adult, Oxidative Stress, Neuroprotective Agents, Animals, Humans, Deferiprone, Female, News & Views
Abstract

International audience; Iron accumulation has been observed in mouse models and in both sporadic and familial forms of amyotrophic lateral sclerosis (ALS). Iron chelation could reduce iron accumulation and the related excess of oxidative stress in the motor pathways. However, classical iron chelation would induce systemic iron depletion. We assess the safety and efficacy of conservative iron chelation (i.e., chelation with low risk of iron depletion) in a murine preclinical model and pilot clinical trial. In Sod1 mice, deferiprone increased the mean life span compared with placebo. The safety was good, without anemia after 12 months of deferiprone in the 23 ALS patients enrolled in the clinical trial. The decreases in the ALS Functional Rating Scale and the body mass index were significantly smaller for the first 3 months of deferiprone treatment (30 mg/kg/day) than for the first treatment-free period. Iron levels in the cervical spinal cord, medulla oblongata, and motor cortex (according to magnetic resonance imaging), as well as cerebrospinal fluid levels of oxidative stress and neurofilament light chains were lower after deferiprone treatment. Our observation leads to the hypothesis that moderate iron chelation regimen that avoids changes in systemic iron levels may constitute a novel therapeutic modality of neuroprotection for ALS. Antioxid. Redox Signal. 29, 742-748.

Published
2018

30. Genetic and epigenetic alterations in normal and sensitive COPD-diseased human bronchial epithelial cells repeatedly exposed to air pollution-derived PM 2.5

Author

Leclercq, B., primary, Platel, A., additional, Antherieu, S., additional, Alleman, L.Y., additional, Hardy, E.M., additional, Perdrix, E., additional, Grova, N., additional, Riffault, V., additional, Appenzeller, B.M., additional, Happillon, M., additional, Nesslany, F., additional, Coddeville, P., additional, Lo-Guidice, J-M., additional, and Garçon, G., additional

Published
2017
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31. Développement et validation de méthodes pour l’analyse de la composition chimique des e-liquides et de leurs e-vapeurs, et comparaison à la fumée de cigarette conventionnelle

Author

Beauval, N., primary, Antherieu, S., additional, Soyez, M., additional, Gengler, N., additional, Grova, N., additional, Howsam, M., additional, Hardy, E., additional, Fischer, M., additional, Appenzeller, B., additional, Goossens, J.-F., additional, Allorge, D., additional, Garçon, G., additional, Lo-Guidice, J.-M., additional, and Garat, A., additional

Published
2017
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32. Differential responses of healthy and chronic obstructive pulmonary diseased human bronchial epithelial cells repeatedly exposed to air pollution-derived PM4

Author

Leclercq, B., primary, Happillon, M., additional, Antherieu, S., additional, Hardy, E.M., additional, Alleman, L.Y., additional, Grova, N., additional, Perdrix, E., additional, Appenzeller, B.M., additional, Lo Guidice, J.-M., additional, Coddeville, P., additional, and Garçon, G., additional

Published
2016
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36. Évaluation des risques sanitaires liés à l’utilisation professionnelle des produits bitumineux et de leurs additifs – Résultats de l’expertise collective – Conclusions et recommandations de l’Anses

Author

Fourneau, C., primary, Boulanger, G., additional, Nerriere-Catelinois, E., additional, Cointot, M.-L., additional, Argiles, G., additional, Stücker, I., additional, Lafontaine, M., additional, Cesarini, J.-P., additional, Huynh, C.K., additional, Garçon, G., additional, Appenzeller, B., additional, Schroeder, H., additional, Sutter, B., additional, and Bourgeois, D., additional

Published
2014
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46. Mutagenicity and genotoxicity of PM.

Author

André, V., Billet, S., Pottier, D., Le Goff, J., Pottier, I., Garçon, G., Shirali, P., and Sichel, F.

Subjects
MUTAGENICITY testing, CHRONIC toxicity testing, POLYCYCLIC aromatic hydrocarbons, LUNG cancer, CELLS, MUTAGENS, NITROAROMATIC compounds, AROMATIC compounds
Abstract

Epidemiological studies have demonstrated the link between chronic exposure to particulate matter (PM), especially particles with an aerodynamic diameter lesser than 2.5 µm (PM), and lung cancer. Mechanistic investigations focus on the contribution of the various genotoxicants adsorbed onto the particles, and more particularly on polycyclic aromatic hydrocarbons or nitroaromatics. Most of the previous studies dealing with genotoxic and/or mutagenic measurements were performed on organic extracts obtained from PM collected in polluted areas. In contrast, we have evaluated genotoxic and mutagenic properties of urbano-industrial PM (PM) collected in Dunkerque (France). Thermally desorbed PM (dPM) was also comparatively studied. Suspensions of PM and dPM (5-50 µg per plate) were tested in Salmonella tester strains TA98, TA102 and YG1041 ± S9mix. Significant mutagenicity was observed for PM in YG1041 ± S9 mix. In strain TA102 - S9mix, a slight, but not significant dose-response increase was observed, for both PM and dPM. Genotoxic properties of PM and dPM were evaluated by the measurement of (1) 8-OHdG in A549 cells and (2) bulky DNA adducts on A549 cells and on human alveolar macrophages (AMs) in primary culture. A dose-dependant formation of 8-OHdG adducts was observed on A549 cells for PM and dPM, probably mainly attributed to the core of the particles. Bulky DNA adducts were observed only in AMs after exposure to PM and dPM. In conclusion, using relevant exposure models, suspension of PM induces a combination of DNA-interaction mechanisms, which could contribute to the induction of lung cancer in exposed populations. Copyright © 2010 John Wiley & Sons, Ltd. Genotoxic and mutagenic properties of suspensions of PM (PM) collected in Dunkerque (France) were evaluated together with their thermally desorbed counterpart (dPM). Significant mutagenicity was observed for PM only in Salmonella tester strains YG1041 ± S9 mix. For PM and dPM, a slight dose-response increase was observed in strain TA102 - S9mix. PM and dPM induced 8-OHdG adducts formation on A549 cells in a dose-dependent manner, together with bulky DNA adducts on human alveolar macrophages in primary culture. [ABSTRACT FROM AUTHOR]

Published
2011
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47. Environmental lead exposure and its relationship to traffic density among Senegalese children: a pilot study.

Author

Diouf, A., Garçon, G., Thiaw, C., Diop, Y., Fall, M., Ndiaye, B., Siby, T., Hannothiaux, M. H., Zerimech, F., Ba, D., Haguenoer, J. M., and Shirali, P.

Subjects
*KIDNEY diseases, *POLLUTION, *ENVIRONMENTAL quality, *LEAD abatement, *POLLUTION laws, *AIR pollution, *AIR pollution potential, *ACUTE kidney failure, *ECOLOGY
Abstract

In Senegal, as in many developing countries, traffic density is increasing in urban areas; in Dakar more than 50% of vehicles use gasoline. Yet the extent and real magnitude of the problem has neither been recognized nor assessed in these countries. Systemic data assessment of lead pollution and people's exposure are not well known in Senegal. This study was also designed to determine the impregnation levels of the lead released by the exhaust of cars and the changes of some early biological markers in Senegalese children. Blood lead (BPb) levels showed that all the children enrolled were exposed. However, lead exposure levels (from 34.7 to 145.8 μg/L) were less important for children living in rural areas (60.9 ± 18.3 μg/L) than for those living in urban areas (106.7 ± 16.9 μg/L). These changes could be correlated to the difference in the automobile traffic between both these regions (P < 0.001). BPb mean levels found in boys were higher than those in girls (P < 0.05). Despite elevated BPb levels, all values for blood zinc protoporphyrin and urine delta-aminolevulinic acid were within physiological ranges. In addition, variations in some biological markers of oxidative stress and renal disorders were seen; however, they must be confirmed by a future epidemiological study. [ABSTRACT FROM AUTHOR]

Published
2003
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