Oxidative stress pathways involved in cytotoxicity and genotoxicity of titanium dioxide (TiO2) nanoparticles on cells constitutive of alveolo-capillary barrier in vitro
The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidativ...
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| Veröffentlicht in: | Toxicology in vitro Jg. 33; S. 125 - 135 |
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01.06.2016
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| Abstract | The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidative stress. To investigate this problem further, the effect of titanium dioxide nanoparticles was examined on cell lines representative of alveolo-capillary barrier.
The present study showed that all nanoparticle-exposed cell lines displayed ROS generation. Macrophage-like THP-1 and HPMEC-ST1.6R microvascular cells were sensitive to endogenous redox changes and underwent apoptosis, but not alveolar epithelial A549 cells. Genotoxic potential of titanium dioxide nanoparticles was investigated using the activation of γH2AX, activation of DNA repair proteins and cell cycle arrest. In the sensitive cell lines, DNA damage was persistent and activation of DNA repair pathways was observed. Moreover, western blot analysis showed that specific pathways associated with cellular stress response were activated concomitantly with DNA repair or apoptosis.
Nanoparticles-induced oxidative stress is finally signal transducer for further physiological effects including genotoxicity and cytotoxicity. Within activated pathways, HSP27 and SAPK/JNK proteins appeared as potential biomarkers of intracellular stress and of sensitivity to endogenous redox changes, respectively, enabling to predict cell behavior.
•Nanoparticle-exposed cell lines showed ROS generation, a common toxicity mechanism.•Alveolar epithelial A549 were resistant to nanoparticle exposure.•HPMEC-ST1.6R and THP-1 cells were sensitive to endogenous redox changes.•Correlation between cyto- and geno-toxicological endpoints and oxidative stress activated pathways•HSP27 and SAPK/JNK proteins were potential markers to predict cell response. |
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| AbstractList | The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidative stress. To investigate this problem further, the effect of titanium dioxide nanoparticles was examined on cell lines representative of alveolo-capillary barrier. The present study showed that all nanoparticle-exposed cell lines displayed ROS generation. Macrophage-like THP-1 and HPMEC-ST1.6R microvascular cells were sensitive to endogenous redox changes and underwent apoptosis, but not alveolar epithelial A549 cells. Genotoxic potential of titanium dioxide nanoparticles was investigated using the activation of γH2AX, activation of DNA repair proteins and cell cycle arrest. In the sensitive cell lines, DNA damage was persistent and activation of DNA repair pathways was observed. Moreover, western blot analysis showed that specific pathways associated with cellular stress response were activated concomitantly with DNA repair or apoptosis. Nanoparticles-induced oxidative stress is finally signal transducer for further physiological effects including genotoxicity and cytotoxicity. Within activated pathways, HSP27 and SAPK/JNK proteins appeared as potential biomarkers of intracellular stress and of sensitivity to endogenous redox changes, respectively, enabling to predict cell behavior. The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidative stress. To investigate this problem further, the effect of titanium dioxide nanoparticles was examined on cell lines representative of alveolo-capillary barrier. The present study showed that all nanoparticle-exposed cell lines displayed ROS generation. Macrophage-like THP-1 and HPMEC-ST1.6R microvascular cells were sensitive to endogenous redox changes and underwent apoptosis, but not alveolar epithelial A549 cells. Genotoxic potential of titanium dioxide nanoparticles was investigated using the activation of gamma H2AX, activation of DNA repair proteins and cell cycle arrest. In the sensitive cell lines, DNA damage was persistent and activation of DNA repair pathways was observed. Moreover, western blot analysis showed that specific pathways associated with cellular stress response were activated concomitantly with DNA repair or apoptosis. Nanoparticles-induced oxidative stress is finally signal transducer for further physiological effects including genotoxicity and cytotoxicity. Within activated pathways, HSP27 and SAPK/JNK proteins appeared as potential biomarkers of intracellular stress and of sensitivity to endogenous redox changes, respectively, enabling to predict cell behavior. The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidative stress. To investigate this problem further, the effect of titanium dioxide nanoparticles was examined on cell lines representative of alveolo-capillary barrier. The present study showed that all nanoparticle-exposed cell lines displayed ROS generation. Macrophage-like THP-1 and HPMEC-ST1.6R microvascular cells were sensitive to endogenous redox changes and underwent apoptosis, but not alveolar epithelial A549 cells. Genotoxic potential of titanium dioxide nanoparticles was investigated using the activation of γH2AX, activation of DNA repair proteins and cell cycle arrest. In the sensitive cell lines, DNA damage was persistent and activation of DNA repair pathways was observed. Moreover, western blot analysis showed that specific pathways associated with cellular stress response were activated concomitantly with DNA repair or apoptosis. Nanoparticles-induced oxidative stress is finally signal transducer for further physiological effects including genotoxicity and cytotoxicity. Within activated pathways, HSP27 and SAPK/JNK proteins appeared as potential biomarkers of intracellular stress and of sensitivity to endogenous redox changes, respectively, enabling to predict cell behavior.The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidative stress. To investigate this problem further, the effect of titanium dioxide nanoparticles was examined on cell lines representative of alveolo-capillary barrier. The present study showed that all nanoparticle-exposed cell lines displayed ROS generation. Macrophage-like THP-1 and HPMEC-ST1.6R microvascular cells were sensitive to endogenous redox changes and underwent apoptosis, but not alveolar epithelial A549 cells. Genotoxic potential of titanium dioxide nanoparticles was investigated using the activation of γH2AX, activation of DNA repair proteins and cell cycle arrest. In the sensitive cell lines, DNA damage was persistent and activation of DNA repair pathways was observed. Moreover, western blot analysis showed that specific pathways associated with cellular stress response were activated concomitantly with DNA repair or apoptosis. Nanoparticles-induced oxidative stress is finally signal transducer for further physiological effects including genotoxicity and cytotoxicity. Within activated pathways, HSP27 and SAPK/JNK proteins appeared as potential biomarkers of intracellular stress and of sensitivity to endogenous redox changes, respectively, enabling to predict cell behavior. The health risks of nanoparticles remain a serious concern given their prevalence from industrial and domestic use. The primary route of titanium dioxide nanoparticle exposure is inhalation. The extent to which nanoparticles contribute to cellular toxicity is known to associate induction of oxidative stress. To investigate this problem further, the effect of titanium dioxide nanoparticles was examined on cell lines representative of alveolo-capillary barrier. The present study showed that all nanoparticle-exposed cell lines displayed ROS generation. Macrophage-like THP-1 and HPMEC-ST1.6R microvascular cells were sensitive to endogenous redox changes and underwent apoptosis, but not alveolar epithelial A549 cells. Genotoxic potential of titanium dioxide nanoparticles was investigated using the activation of γH2AX, activation of DNA repair proteins and cell cycle arrest. In the sensitive cell lines, DNA damage was persistent and activation of DNA repair pathways was observed. Moreover, western blot analysis showed that specific pathways associated with cellular stress response were activated concomitantly with DNA repair or apoptosis. Nanoparticles-induced oxidative stress is finally signal transducer for further physiological effects including genotoxicity and cytotoxicity. Within activated pathways, HSP27 and SAPK/JNK proteins appeared as potential biomarkers of intracellular stress and of sensitivity to endogenous redox changes, respectively, enabling to predict cell behavior. •Nanoparticle-exposed cell lines showed ROS generation, a common toxicity mechanism.•Alveolar epithelial A549 were resistant to nanoparticle exposure.•HPMEC-ST1.6R and THP-1 cells were sensitive to endogenous redox changes.•Correlation between cyto- and geno-toxicological endpoints and oxidative stress activated pathways•HSP27 and SAPK/JNK proteins were potential markers to predict cell response. |
| Author | Hanot-Roy, Maïté Guilbert, Ariane Tubeuf, Emilie Braun, Anne Lacroix, Ghislaine Trouiller, Bénédicte Vigneron, Pascale Bado-Nilles, Anne |
| Author_xml | – sequence: 1 givenname: Maïté orcidid: 0000-0002-7104-5973 surname: Hanot-Roy fullname: Hanot-Roy, Maïté email: maite.hanot@free.fr organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France – sequence: 2 givenname: Emilie surname: Tubeuf fullname: Tubeuf, Emilie organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France – sequence: 3 givenname: Ariane surname: Guilbert fullname: Guilbert, Ariane organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France – sequence: 4 givenname: Anne surname: Bado-Nilles fullname: Bado-Nilles, Anne organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité d'Ecotoxicologie in vitro et in vivo, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France – sequence: 5 givenname: Pascale surname: Vigneron fullname: Vigneron, Pascale organization: Université de Technologie de Compiègne (UTC), Laboratoire BioMécanique et BioIngénierie (BMBI), UMR CNRS 7338, 60205 Compiègne, France – sequence: 6 givenname: Bénédicte surname: Trouiller fullname: Trouiller, Bénédicte organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France – sequence: 7 givenname: Anne surname: Braun fullname: Braun, Anne organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France – sequence: 8 givenname: Ghislaine surname: Lacroix fullname: Lacroix, Ghislaine organization: Institut National de l'Environnement Industriel et des Risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA-BP 2, F-60550 Verneuil-en-Halatte, France |
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| SubjectTerms | Apoptosis - drug effects Capillaries Cell Cycle Checkpoints - drug effects Cell death Cell Line Cell Line, Tumor Cell Survival - drug effects DNA Damage DNA repair Ecotoxicology Glutathione - metabolism Histones - metabolism HSP27 Heat-Shock Proteins - metabolism Humans Life Sciences Metal Nanoparticles - toxicity Nanotoxicology Oxidative stress Oxidative Stress - drug effects p38 Mitogen-Activated Protein Kinases - metabolism Pulmonary Alveoli Reactive Oxygen Species - metabolism Titanium - toxicity Toxicology |
| Title | Oxidative stress pathways involved in cytotoxicity and genotoxicity of titanium dioxide (TiO2) nanoparticles on cells constitutive of alveolo-capillary barrier in vitro |
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