Gene expression profiling of A549 cells exposed to Milan PM2.5

Gualtieri, Maurizio; Longhin, Eleonora; Mattioli, Michela; Mantecca, Paride; Tinaglia, Valentina; Mangano, Eleonora; Proverbio, Maria Carla; Bestetti, Giuseppina; Camatini, Marina; Battaglia, Cristina

doi:10.1016/j.toxlet.2011.11.015

Cited by 130 publications

(86 citation statements)

References 58 publications

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“…Oxidative DNA damage in lung cells has been extensively reported in in vitro and in vivo systems exposed to PM or UFPs (Gualtieri et al, 2012;Longhin et al, 2013;Meng and Zhang, 2007;Oh et al, 2011). Pb, a prevalent toxic metal component in ambient PM, is known to induce oxidative stress and oxidative DNA damage.…”

Section: Discussionmentioning

confidence: 99%

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Yuan

et al. 2015

Ecotoxicology and Environmental Safety

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Section: Discussionmentioning

confidence: 99%

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Yuan

et al. 2015

Ecotoxicology and Environmental Safety

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“…Aerosols may carry of acidic or toxic species and may have detrimental effects on human health and ecosystems (Cheng et al, 1996). Human health endpoints associated with exposure to aerosols include increased mortality and pulmonary and cardiovascular diseases (Lee et al, 2006;Perrone et al, 2010;Gualtieri et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Seasonal Behaviours and Weekdays/Weekends Differences in Elemental Composition of Atmospheric Aerosols in Cairo, Egypt

Hassan

El–Abssawy

Abdelmaksoud

et al. 2013

Aerosol Air Qual. Res.

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The aim of the present study was to investigate the seasonal distributions and weekdays/weekends differences in ambient aerosols and their elemental contents in the atmosphere of the 15 May City, Egypt. Aerosol samples were collected from March 2009 to February 2010. The concentrations of 14 elements including Na, Mg, Ca, K, Al, Fe, Mn, Co, Cu, Zn, Ni, Cd, Pb and Cr were measured by Atomic Absorption Spectrophotometry (AAS). The mean aerosols concentrations were 290 µg/m 3 (spring), 250 µg/m 3 (summer), 330 µg/m 3 (autumn) and 400 µg/m 3 (winter). The measured elements showed a strong seasonal variation; with the highest concentrations in winter and the lowest in summer. Na, Mg, Ca, K, Al and Fe were the dominant elements, followed by Mn, Cu, Zn, Ni and Pb. The minimum concentrations were noted for Co, Cd and Cr. The dominant elements in aerosol represented 94%, 94.51%, 94.61% and 94.28% from the total measured elements and 5.08%, 5.74%, 6.11% and 5.44% from aerosol mass during winter, spring, summer and autumn, respectively. The aerosols concentrations on weekends were reduced by 31.25% in the winter and 15.2% in the summer. The concentrations of the measured elements were higher on weekdays than weekends. The weekday/weekend concentration ratios were 1.69 and 1.38 for total measured elements during winter and summer, respectively. The mean Ni and Cd levels were higher than the proposed WHO, USEPA and the European Community standards. Significant positive correlations were found between the concentrations of aerosols, Mg, Ca, K, Al, Fe, Mn, Co, Zn and Cr. The enrichment factors (EFs) and the non-crustal fractions of all elements indicated that Na, Mg, Ca, K, Fe and Mn originate mainly from soil sources, whereas Co, Cu, Zn, Ni, Cd, Pb and Cr are mostly emitted in the atmosphere of 15 May City from anthropogenic sources.

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“…Notably, the capability of PM in inducing cell damage may diverse due to different locations and seasons. For instance, winter Milan PM 2.5 induces a higher degree of DNA damage in comparison with summer PM 2.5 [10]. Therefore, "standard" PM, which has been collected and analyzed by the National Institute for 18 h according to a previous study [15].…”

Section: Introductionmentioning

confidence: 99%

“…The biological characterization of the Standard Reference Material 1648 for PM 10 (SRM 1648) in epithelial cells has been reported [11], but the effect of SRM 2786 for fine PM on bronchial epithelial cell growth has not yet been evaluated. The proliferation of bronchial epithelial cells has also been affected by various micro-environmental factors except direct damage caused by PM, including inflammation.…”

mentioning

confidence: 99%

Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

Xiong

Chen

et al. 2017

Int J Occup Med Environ Health

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Objectives: The aim of the study has been to investigate the effect of the Standard Reference Material of fine particulate matter (SRM 2786) on cytotoxicity and apoptosis in human lung bronchial epithelial cells (16HBE cells). Whether the lipopolysaccharide (LPS)-induced inflammation could further accelerate cell apoptosis induced by SRM 2786 stimulation has also been determined. Material and Methods: 16HBE cells were exposed to various doses of SRM 2786 with or without LPS. The following parameters: cytotoxicity, apoptotic rate, Bax/Bcl-2 expression, nitric oxide (NO) production, and reactive oxygen species (ROS) generation were measured. Results: The results have shown that SRM 2786 induces cell damage and apoptosis of 16HBE cells as demonstrated by significant decrease in expression of Bcl-2 and increase in expression of Bax. When compared with the control cells, the apoptotic rate of cells treated by 500 μg/ml of SRM 2786 increased from 2.43±0.21% to 43.96±2.95% (p < 0.01). Further, there was an elevated production of NO and ROS post SRM 2786 treatment. The level of NO in cells treated with 500 μg/ml of SRM 2786 was 18.33±1.02 μmol/l whereas that of control cells was 1.58±0.31 μmol/l (p < 0.01). When compared with the control group, the level of intracellular ROS increased by 24% after treatment with 500 μg/ml of SRM 2786 (p < 0.05). In addition, LPS pre-treatment may accelerate cell apoptosis by increasing generation of NO and ROS followed by SRM 2786 stimulation. When compared to cells treated with 125 μg/ml of SRM 2786 alone, the levels of NO and ROS in cells pretreated with LPS increased by 28% and 11.6%, respectively (p < 0.05), and the apoptotic rate increased from 34.62±4.44% to 54.11±3.34% (p < 0.01). Conclusions: These findings have suggested that in vitro exposure to SRM 2786 could induce 16HBE cells apoptosis probably by means of the mechanism involving the generation of free radicals, while the degree of apoptosis would be further aggravated under inflammation condition. Int J Occup Med Environ Health 2018;31(2):173 -183

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Gene expression profiling of A549 cells exposed to Milan PM2.5

Cited by 130 publications

References 58 publications

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Seasonal Behaviours and Weekdays/Weekends Differences in Elemental Composition of Atmospheric Aerosols in Cairo, Egypt

Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

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