Presentation Type
Poster
Keywords
Biology, inositol triphosphate, apoptosis, human alveolar lung cells, nanoparticles, stress signaling
Department
Biology
Major
Biology
Abstract
The signaling of cell stress in response to organelle dysfunction, toxin exposure, and mutation is complex; generating responses that can include adaptation, or in severe cases, cellular apoptosis. Nanoparticles (20-100 nm diameter) have been shown to induce cell stress in lung cells, potentially identifying a cause of lung disease in areas with high levels of particulate-based air pollution. This study examines the effect of carbon black (CB) and titanium dioxide (TiO2) nanoparticles on stress signaling and apoptosis in cultured A549 human alveolar epithelial cells. CB and TiO2 powders were dispersed throughout a buffered solution containing bovine serum albumin using probe sonication. Particle size analysis was performed, revealing stable nanoparticle complexes ranging from 75 nm for CB and from 172 nm for TiO2. A range of nanoparticle doses between 5 and 100 μg/mL were evaluated for toxicity using a visual inspection for DAPI-stained apoptotic nuclei. This assay revealed a peak of cell death activation at 75 μg/mL for CB and 100 μg/mL for TiO2 though the CB was more effective at inducing apoptosis than TiO2. A live/dead-cell fluorescent protease assay confirmed CB to significantly decrease cell viability. Further studies revealed acute CB exposure, but not TiO2 exposure, to induce reactive oxygen species (ROS). Interestingly, inhibition of nanoparticle-induced calcium release by the inositol triphosphate receptor (ITPR) inhibited ROS production, suggesting a role for ER Ca2+ stores in activating ROS production. Further research is underway to determine which stress/apoptotic signaling pathways are induced downstream of nanoparticle exposure.
Faculty Mentor
Jay Brewster
Funding Source or Research Program
Summer Undergraduate Research Program, Undergraduate Research Fellowship
Location
Waves Cafeteria, Tyler Campus Center
Start Date
21-3-2014 2:00 PM
End Date
21-3-2014 3:00 PM
Included in
Nanoparticle exposure activates an inositol triphosphate receptor-dependent elevation of reactive oxygen species and apoptosis in human alveolar lung cells
Waves Cafeteria, Tyler Campus Center
The signaling of cell stress in response to organelle dysfunction, toxin exposure, and mutation is complex; generating responses that can include adaptation, or in severe cases, cellular apoptosis. Nanoparticles (20-100 nm diameter) have been shown to induce cell stress in lung cells, potentially identifying a cause of lung disease in areas with high levels of particulate-based air pollution. This study examines the effect of carbon black (CB) and titanium dioxide (TiO2) nanoparticles on stress signaling and apoptosis in cultured A549 human alveolar epithelial cells. CB and TiO2 powders were dispersed throughout a buffered solution containing bovine serum albumin using probe sonication. Particle size analysis was performed, revealing stable nanoparticle complexes ranging from 75 nm for CB and from 172 nm for TiO2. A range of nanoparticle doses between 5 and 100 μg/mL were evaluated for toxicity using a visual inspection for DAPI-stained apoptotic nuclei. This assay revealed a peak of cell death activation at 75 μg/mL for CB and 100 μg/mL for TiO2 though the CB was more effective at inducing apoptosis than TiO2. A live/dead-cell fluorescent protease assay confirmed CB to significantly decrease cell viability. Further studies revealed acute CB exposure, but not TiO2 exposure, to induce reactive oxygen species (ROS). Interestingly, inhibition of nanoparticle-induced calcium release by the inositol triphosphate receptor (ITPR) inhibited ROS production, suggesting a role for ER Ca2+ stores in activating ROS production. Further research is underway to determine which stress/apoptotic signaling pathways are induced downstream of nanoparticle exposure.