title: Oxidative stress and inflammatory response to printer toner particles in human epithelial A549 lung cells.
abstract: Reports on adverse health effects related to occupational exposure to toner powder are still inconclusive. Therefore, we have previously conducted an in vitro-study to characterize the genotoxic potential of three commercially available black printer toner powders in A549 lung cells. In these cell-based assays it was clearly demonstrated that the tested toner powders damage DNA and induce micronucleus (MN) formation. Here, we have studied the cytotoxic and proinflammatory potential of these three types of printer toner particles and the influence of ROS and NF-κB induction in order to unravel the underlying mechanisms. A549 cells were exposed to various concentrations of printer toner particle suspensions for 24 h. The toner particles were observed to exert significant cytotoxic effects in the WST-1 and neutral red (NR)-assays, although to a varying extent. Caspase 3/7 activity increased, while the mitochondrial membrane potential (MMP) was not affected. Particles of all three printer toner powders induced concentration-dependent formation of reactive oxygen species (ROS), as measured in the DCFH-DA assay. Furthermore, toner particle exposure enhanced interleukin-6 and interleukin-8 production, which is in agreement with activation of the transcription factor NF-κB in A549 cells shown by the electrophoretic mobility shift assay (EMSA). Therefore, it can be concluded that exposure of A549 lung cells to three selected printer toner powders caused oxidative stress through induction of ROS. Increased ROS formation may trigger genotoxic effects and activate proinflammatory pathways.
authors.affiliation: Department of Environmental Health Sciences, University Medical Center Freiburg, Freiburg, Germany. mathias.koenczoel@pharmazie.uni-freiburg.de
authors.forename: Mathias
authors.initials: M
authors.lastname: Könczöl
authors.forename: Adilka
authors.initials: A
authors.lastname: Weiß
authors.forename: Richard
authors.initials: R
authors.lastname: Gminski
authors.forename: Irmgard
authors.initials: I
authors.lastname: Merfort
authors.forename: Volker
authors.initials: V
authors.lastname: Mersch-Sundermann
mesh_terms: D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D024202:Electrophoretic Mobility Shift Assay; D005290:Ferric Compounds / Q000633:toxicity*; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D016328:NF-kappa B / Q000378:metabolism; D009499:Neutral Red / Q000737:chemistry; D018384:Oxidative Stress / Q000187:drug effects*; D010316:Particle Size; D011014:Pneumonia / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013778:Tetrazolium Salts / Q000737:chemistry
chemical_list: C110656:2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium; D005290:Ferric Compounds; D015850:Interleukin-6; D016209:Interleukin-8; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D013778:Tetrazolium Salts; C000499:ferric oxide; D009499:Neutral Red; D020169:Caspases