Assessment of DNA Damage and Cell Senescence in Corneal Epithelial Cells Exposed to Airborne Particulate Matter (PM2.5) Collected in Guangzhou, China
| Autor: | Zhi-Jie Li, Yu-Hong Cui, Zi-Xun Gao, Guang Yang, Shan-Shan Li, Xi-Ling Song, Hong-Wei Pan, Yu-Lan Yang, Xiao-Rong Lai |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Senescence China Pathology medicine.medical_specialty Cell Survival DNA damage DNA repair Cell 010501 environmental sciences Biology 01 natural sciences 03 medical and health sciences Air Pollution medicine Animals Humans Viability assay Cells Cultured Cellular Senescence 0105 earth and related environmental sciences Corneal epithelium chemistry.chemical_classification Reactive oxygen species Epithelium Corneal Epithelial Cells Molecular biology 030104 developmental biology medicine.anatomical_structure chemistry Cattle Particulate Matter Reactive Oxygen Species Cell aging DNA Damage |
| Zdroj: | Investigative Opthalmology & Visual Science. 57:3093 |
| ISSN: | 1552-5783 |
| Popis: | Purpose To assess the genotoxic effect of airborne particulate matter on corneal epithelial cells and investigate the role of reactive oxygen species (ROS) formation in this process. Methods Immortalized human corneal epithelial cells (HCECs) and primary bovine corneal epithelial cells were exposed to airborne particulate matter collected from Guangzhou for 24 hours. The cell viability and toxicity were measured by the CCK-8 test and lactate dehydrogenase (LDH) release, respectively. The DNA breaks and DNA repair were examined by alkaline comet assay and by immunofluorescence staining of the phosphorylated histone variant H2AX (γH2AX), respectively. Reactive oxygen species production was assessed by the fluorescent probe, CM-H2DCFDA. Cell senescence was evaluated with senescence-associated β-Galactosidase staining, and cell ultrastructure was observed with transmission electron microscopy. Results Exposure to PM2.5 at the concentration of 20 μg/mL to 200 μg/mL decreased cell viability and increased LDH release. Remarkably increased DNA double-stand breaks, increased expression of DNA repair-related protein γH2AX, elevated ROS formation, and altered cell ultrastructure were observed in HCECs after treatment with PM2.5. The genotoxic effect of PM2.5 was attenuated by the ROS inhibitor N-acetyl-l-cysteine (NAC). Conclusions Particulate matter 2.5 could induce DNA damage and cell senescence in corneal epithelial cells, probably by promoting ROS formation. Thus, whether long-term exposure of PM2.5 might be related to potential risk of abnormality in corneal epithelium renewal and regeneration should be further investigated. |
| Databáze: | OpenAIRE |
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