Clothianidin induces DNA damage and oxidative stress in bronchial epithelial cells

2020 ◽  
Vol 61 (6) ◽  
pp. 647-655 ◽  
Author(s):  
Zülal Atlı Şekeroğlu ◽  
Vedat Şekeroğlu ◽  
Birsen Aydın ◽  
Seval Kontaş Yedier ◽  
Emre İlkun
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
And Oxidative Stress

scholarly journals Effects of DNA Damage and Oxidative Stress in Human Bronchial Epithelial Cells Exposed to PM2.5 from Beijing, China, in Winter

2020 ◽  
Vol 17 (13) ◽  
pp. 4874 ◽  
Author(s):  
Bing-Yu Niu ◽  
Wen-Ke Li ◽  
Jiang-Shuai Li ◽  
Qi-Hao Hong ◽  
Sara Khodahemmati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Repair Gene ◽  
Bronchial Epithelial ◽  
Dna Repair Gene ◽  
Pm2.5 Exposure

Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter (<2.5 μm) (PM2.5) exposure. The toxic responses of PM2.5 are greatly influenced by the source of PM2.5. However, the effects of PM2.5 from Beijing on bronchial genotoxicity are scarce. In the present study, PM2.5 from Beijing was sampled and applied in vitro to investigate its genotoxicity and the mechanisms behind it. Human bronchial epithelial cells 16HBE were used as a model for exposure. Low (67.5 μg/mL), medium (116.9 μg/mL), and high (202.5 μg/mL) doses of PM2.5 were used for cell exposure. After PM2.5 exposure, cell viability, oxidative stress markers, DNA (deoxyribonucleic acid) strand breaks, 8-OH-dG levels, micronuclei formation, and DNA repair gene expression were measured. The results showed that PM2.5 significantly induced cytotoxicity in 16HBE. Moreover, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and cellular heme oxygenase (HO-1) were increased, and the level of glutathione (GSH) was decreased, which represented the occurrence of severe oxidative stress in 16HBE. The micronucleus rate was elevated, and DNA damage occurred as indicators of the comet assay, γ-H2AX and 8-OH-dG, were markedly enhanced by PM2.5, accompanied by the influence of 8-oxoguanine DNA glycosylase (OGG1), X-ray repair cross-complementing gene 1 (XRCC1), and poly (ADP-ribose) polymerase-1 (PARP1) expression. These results support the significant role of PM2.5 genotoxicity in 16HBE cells, which may occur through the combined effect on oxidative stress and the influence of DNA repair genes.

Etomidate Regulates miR-192-5p Expression to Reduce Hypoxia-Reoxygenation Induced Bronchial Epithelial Cell Damage

2021 ◽  
Vol 11 (3) ◽  
pp. 458-465
Author(s):  
Tian Xia ◽  
Yang Cao ◽  
Jinxiu Li ◽  
Xin Zhang ◽  
Guangyuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Protein Level ◽  
Cell Damage ◽  
Bronchial Epithelial Cells ◽  
Sod Activity ◽  
Bronchial Epithelial ◽  
Apoptosis Rate ◽  
And Oxidative Stress ◽  
Hypoxia Reoxygenation

Etomidate is a new type of intravenous anesthetic that can protect bronchial epithelial cells from oxidative stress damage. miR-192-5p is upregulated in 6-hydroxydopamine-induced neurocytes. This study explored the effect of etomidate on bronchial epithelial cell apoptosis and oxidative stress induced by hypoxia and reoxygenation and its regulatory effect on miR-192-5p. The human bronchial epithelial cells BEAS-2B were cultured in vitro and then subjected to hypoxia and reoxygenation to establish a cell injury model. The cells were then treated with etomidate at different doses. Moreover, anti-miR-NC and anti-miR-192-5p were transfected into the BEAS-2B cells to treat the hypoxia-reoxygenation. Moreover, miR-NC and miR-192-5p mimics were transfected into BEAS-2B cells, followed by treatment with 90 µmol/L etomidate for 24 h and then treatment with hypoxia and reoxygenation. The 2,4-dinitrophenylhydrazine method was used to determine the level of LDH in the culture medium of cardiomyocytes. Thiobarbituric acid was used to determine the level of MDA and xanthine oxidase to determine the activity of SOD. Flow cytometry was used to measure the apoptosis rate and qRT-PCR to evaluate miR-192-5p expression. Western blotting was used to determine the Bax and Bcl-2 protein levels. Compared with the findings in the control group, the levels of LDH and MDA, the apoptosis rate, and the protein level of Bax were increased (P < 0.05) upon treatment with hypoxia and reoxygenation, while SOD activity and Bcl-2 protein level were decreased (P < 0.05). In a manner dependent on the dose, etomidate could significantly reverse the effects of hypoxia and reoxygenation on oxidative stress and apoptosis of BEAS-2B cells (P < 0.05). Hypoxia and reoxygenation could significantly increase the miR-192-5p level of BEAS-2B cells (P < 0.05), while etomidate could reduce this miR-192-5p expression (P < 0.05) in a dose-dependent manner. Transfection of anti-miR-192-5p dramatically reduced LDH, MDA, apoptosis rate, and Bax protein level (P < 0.05), but was associated with increases of SOD activity and Bcl-2 protein expression (P < 0.05). High expression of miR-192-5p could significantly reverse the influence of etomidate on apoptosis and oxidative stress of BEAS-2B cells induced by hypoxia-reoxygenation (P < 0.05). Etomidate restrained the apoptosis of bronchial epithelial cells and oxidative stress induced by hypoxia and reoxygenation by inhibiting miR-192-5p expression, thereby reducing cell damage.

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