PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells

Deng, Xiaobei; Zhang, Fang; Wei, Rui; Long, Fang; Wang, Limin; Zhu, Feng; Chen, Deliang; Ding, Wenjun

doi:10.1016/j.tiv.2013.05.004

Cited by 345 publications

(210 citation statements)

References 39 publications

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“…Además, puede participar en la reacción de Haber-Weiss, catalizando la formación de radicales hidroxilos a partir de peróxido de hidrógeno y anión superóxido 31,32 . Estos radicales hidroxilo generan infiltración de leucocitos, activación de NF-kB, que inducen liberación de citoquinas e inflamación de las vías aéreas, que explicaría el aumento de células totales en el LBA 7,33 .…”

Section: Discussionunclassified

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

et al. 2017

Rev. méd. Chile

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Effect of copper sulphate on the lung damage induced by chronic intermittent exposure to ozone count, proteins, GGT and AP in BALF (p < 0.05). Foamy and pigmented alveolar macrophages were detected in all lungs of these animals (p < 0.001). Conclusions: Intratracheal instillation of a single dose of CuSO 4 in rats previously subjected to a chronic and intermittent exposure to ozone induces a neutrophil pulmonary inflammatory response and cytoplasmic damage in macrophages. (Rev Med Chile 2017; 145: 9-16)

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Section: Discussionunclassified

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

et al. 2017

Rev. méd. Chile

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“…The association would justify the need of further toxicological approach for investigating the biological mechanism of the adverse effect of the PM 2.5 pollution. Although the mechanism underlying the correlation between PM 2.5 exposure and lung cancer has not fully elucidated, PM 2.5 -induced oxidative stress has been considered as an important molecular mechanism of PM 2.5 -mediated toxicity [7]. Harrison et al (2004) [8] found it plausible that known chemical carcinogens are responsible for the lung cancers attributed to PM 2.5 exposure but the possibility should not be ruled out that particulate matter is capable of causing lung cancer independent of the presence of known carcinogens.…”

Section: Discussionmentioning

confidence: 99%

Geographical Analysis of Lung Cancer Mortality Rate and PM2.5 Using Global Annual Average PM2.5 Grids from MODIS and MISR Aerosol Optical Depth

Hu¹,

Baker²

2017

GEP

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Exposure to particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) may increase risk of lung cancer. The repetitive and broad-area coverage of satellites may allow atmospheric remote sensing to offer a unique opportunity to monitor air quality and help fill air pollution data gaps that hinder efforts to study air pollution and protect public health. This geographical study explores if there is an association between PM 2.5 and lung cancer mortality rate in the conterminous USA. Lung cancer (ICD-10 codes C34-C34) death count and population at risk by county were extracted for the period from 2001 to 2010 from the U.S. CDC WONDER online database. The 2001-2010 Global Annual Average PM 2.5 Grids from MODIS and MISR Aerosol Optical Depth dataset was used to calculate a 10 year average PM 2.5 pollution. Exploratory spatial data analyses, spatial regression (a spatial lag and a spatial error model), and spatially extended Bayesian Monte Carlo Markov Chain simulation found that there is a significant positive association between lung cancer mortality rate and PM 2.5 . The association would justify the need of further toxicological investigation of the biological mechanism of the adverse effect of the PM 2.5 pollution on lung cancer. The Global Annual Average PM 2.5 Grids from MODIS and MISR Aerosol Optical Depth dataset provides a continuous surface of concentrations of PM 2.5 and is a useful data source for environmental health research.

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“…The concentration of the used particles (PM 2.5 extracts) for exposure with cells (24 h at 37 C in a humidified atmosphere with 5% CO 2 ) was in a range of 25-100 mg/ml. Cells not exposed were used as negative controls (Deng et al, 2013).…”

Section: Cell Culture and Pm 25 Treatmentmentioning

confidence: 99%

Water-soluble and organic extracts of ambient PM_2.5 in Tehran air: assessment of genotoxic effects on human lung epithelial cells (A549) by the Comet assay

Bandpi¹,

Eslami²,

Shahsavani

et al. 2016

Toxin Reviews

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PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells

Cited by 345 publications

References 39 publications

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

Geographical Analysis of Lung Cancer Mortality Rate and PM2.5 Using Global Annual Average PM2.5 Grids from MODIS and MISR Aerosol Optical Depth

Water-soluble and organic extracts of ambient PM_2.5 in Tehran air: assessment of genotoxic effects on human lung epithelial cells (A549) by the Comet assay

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PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells

Cited by 345 publications

References 39 publications

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

Geographical Analysis of Lung Cancer Mortality Rate and PM2.5 Using Global Annual Average PM2.5 Grids from MODIS and MISR Aerosol Optical Depth

Water-soluble and organic extracts of ambient PM2.5 in Tehran air: assessment of genotoxic effects on human lung epithelial cells (A549) by the Comet assay

Contact Info

Product

Resources

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Water-soluble and organic extracts of ambient PM_2.5 in Tehran air: assessment of genotoxic effects on human lung epithelial cells (A549) by the Comet assay