Nanosize titanium dioxide stimulates reactive oxygen species in brain microglia and damages neurons in vitro
| Autor: | Julianne Tajuba, Thomas C. Long, Susan D. Hester, Preethi Sama, Navid B. Saleh, Carol D. Swartz, Gregory V. Lowry, Bellina Veronesi, Joel S. Parker |
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| Rok vydání: | 2007 |
| Předmět: |
Health
Toxicology and Mutagenesis Dopamine chemistry.chemical_element Biology medicine.disease_cause P25 chemistry.chemical_compound Mice BV2 neurotoxicity medicine Animals oxidative stress Cells Cultured Cell Line Transformed Oligonucleotide Array Sequence Analysis chemistry.chemical_classification Neurons Titanium Reactive oxygen species Microglia titanium dioxide Gene Expression Profiling Research Public Health Environmental and Occupational Health Neurotoxicity Brain Proteins medicine.disease In vitro Rats Neostriatum medicine.anatomical_structure chemistry Biochemistry Gene Expression Regulation Titanium dioxide Biophysics environmental nanotoxicity Reactive Oxygen Species Oxidative stress medicine.drug |
| Zdroj: | Environmental Health Perspectives |
| ISSN: | 0091-6765 |
| Popis: | Titanium dioxide is a widely used nanomaterial whose photo-reactivity suggests that it could damage biological targets (e.g., brain) through oxidative stress (OS).Brain cultures of immortalized mouse microglia (BV2), rat dopaminergic (DA) neurons (N27), and primary cultures of embryonic rat striatum, were exposed to Degussa P25, a commercially available TiO(2) nanomaterial. Physical properties of P25 were measured under conditions that paralleled biological measures.P25 rapidly aggregated in physiological buffer (800-1,900 nm; 25 degrees C) and exposure media (approximately 330 nm; 37 degrees C), and maintained a negative zeta potential in both buffer (-12.2 +/- 1.6 mV) and media (-9.1 +/- 1.2 mV). BV2 microglia exposed to P25 (2.5-120 ppm) responded with an immediate and prolonged release of reactive oxygen species (ROS). Hoechst nuclear stain was reduced after 24-hr (or=100 ppm) and 48-hr (or=2.5 ppm) exposure. Microarray analysis on P25-exposed BV2 microglia indicated up-regulation of inflammatory, apoptotic, and cell cycling pathways and down-regulation of energy metabolism. P25 (2.5-120 ppm) stimulated increases of intracellular ATP and caspase 3/7 activity in isolated N27 neurons (24-48 hr) but did not produce cytotoxicity after 72-hr exposure. Primary cultures of rat striatum exposed to P25 (5 ppm) showed a reduction of immunohistochemically stained neurons and microscopic evidence of neuronal apoptosis after 6-hr exposure. These findings indicate that P25 stimulates ROS in BV2 microglia and is nontoxic to isolated N27 neurons. However, P25 rapidly damages neurons at low concentrations in complex brain cultures, plausibly though microglial generated ROS. |
| Databáze: | OpenAIRE |
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