Dataset Information

Reaction of monocytes to polystyrene and silica nanoparticles in short-term and long-term exposures.

ABSTRACT: Nanoparticles (NPs) are increasingly used in industrial, health and consumer products. In addition to the intended effects, NPs may also cause cell damage. Typical cytotoxicity assays assess short-term effects in adherent cells but do not evaluate longer exposure times and do not focus on cells in suspension. Since NPs are not removed easily from the organism, non-biodegradable NPs may persist in the systemic circulation and affect monocyte function at low concentrations. To mimic this situation, THP-1 monocytes were exposed to low concentrations of plain polystyrene particles (PPP) in different sizes for short (24 h) and prolonged (16 d) time periods. CELLine CL350, a small two-chamber bioreactor, and sub-culturing in flasks were compared regarding prolonged cytotoxicity testing. Uptake rates of the particles, cytotoxicity screening assays, and interleukin secretion were used for the identification of adverse effects. After 24 h, 50 ?g ml-1 20 nm PPP did not affect cellular viability and interleukin secretion, while at higher concentrations the cytotoxicity of PPP (20 nm-500 nm) was correlated to surface area. After 16 d of exposure at 50 ?g ml-1 20 nm PPP, the decrease in cell number and the increase in interleukins were significant. 200 nm PPP, by contrast, caused only minimal effects. Due to lower reproducibility, CELLine proved to be less suitable for the assessment as compared to sub-culturing in flasks. After prolonged exposure, silica Aerosil OX50 particles also were more cytotoxic towards THP-1 monocytes. The data suggest that prolonged exposure to NPs leads to cytotoxicity at low doses and that induction of cell death may be involved in the observed pro-inflammatory action of NPs.

SUBMITTER: Mrakovcic M

PROVIDER: S-EPMC4441011 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Reaction of monocytes to polystyrene and silica nanoparticles in short-term and long-term exposures.

Mrakovcic Maria M Meindl Claudia C Roblegg Eva E Fröhlich Eleonore E

Toxicology research 20140301 2

Nanoparticles (NPs) are increasingly used in industrial, health and consumer products. In addition to the intended effects, NPs may also cause cell damage. Typical cytotoxicity assays assess short-term effects in adherent cells but do not evaluate longer exposure times and do not focus on cells in suspension. Since NPs are not removed easily from the organism, non-biodegradable NPs may persist in the systemic circulation and affect monocyte function at low concentrations. To mimic this situation ...[more]

PMID: 26005565

Similar Datasets

Project description:BackgroundThe impact of nitrogen dioxide (NO2) and particulate matter with an aerodynamic diameter of less than or equal to 2.5. microns (PM2.5) exposures on lung function has been investigated mainly in children and less in adults. Furthermore, it is unclear whether short-term deviations of air pollutant concentration need to be considered in long-term exposure models.ObjectivesThe aims of this study were to investigate the association between short-term air pollution exposure and lung function and to assess whether short-term deviations of air pollutant concentration should be integrated into long-term exposure models.MethodsShort-term (daily averages 0-7 d prior) and long-term (1- and 4-y means) NO2 and PM2.5 concentrations were modeled using satellite, land use, and meteorological data calibrated on ground measurements. Forced expiratory volume within the first second (FEV1) of forced exhalation and forced vital capacity (FVC) were measured during a LuftiBus assessment (2003-2012) and linked to exposure information from the Swiss National Cohort for 36,085 adults (ages 18-95 y). We used multiple linear regression to estimate adjusted associations, and additionally adjusted models of long-term exposures for short-term deviations in air pollutant concentrations.ResultsA 10μg/m3 increase in NO2 and PM2.5 on the day of the pulmonary function test was associated with lower FEV1 and FVC (NO2: FEV1 -8.0 ml [95% confidence interval: -13.4, -2.7], FVC -16.7 ml [-23.4, -10.0]; PM2.5: FEV1 -15.3 ml [-21.9, -8.7], FVC -18.5 ml [-26.5, -10.5]). A 10μg/m3 increase in 1-y mean NO2 was also associated with lower FEV1 (-7.7 ml; -15.9, 0.5) and FVC (-21.6 ml; -31.9, -11.4), as was a 10μg/m3 increase in 1-y mean PM2.5 (FEV1: -42.2 ml; -56.9, -27.5; FVC: -82.0 ml; -100.1, -63.9). These associations were robust to adjustment for short-term deviations in the concentration of each air pollutant.ConclusionsShort- and long-term air pollution exposures were negatively associated with lung function, in particular long-term PM2.5 exposure with FVC. Our findings contribute substantially to the evidence of adverse associations between air pollution and lung function in adults. https://doi.org/10.1289/EHP7529.

Project description:Rationalepopulation-based studies have demonstrated associations between ambient air pollution exposures and mortality, but few have been able to adjust for occupational exposures. Additionally, two studies have observed higher risks in individuals with occupational dust, gas, or fume exposure.Objectiveswe examined the association of ambient residential exposure to particulate matter less than 10 microm in diameter (PM(10)), particulate matter less than 2.5 microm in diameter (PM(2.5)), NO(2), SO(2), and mortality in 53,814 men in the U.S. trucking industry.Methodsexposures for PM(10), NO(2), and SO(2) at each residential address were assigned using models combining spatial smoothing and geographic covariates. PM(2.5) exposures in 2000 were assigned from the nearest available monitor. Single and multipollutant Cox proportional hazard models were used to examine the association of an interquartile range (IQR) change (6 microg/m(3) for PM(10), 4 microg/m(3) for PM(2.5), 4ppb for SO(2), and 8ppb for NO(2)) and the risk of all-cause and cause-specific mortality.Measurements and main resultsan IQR change in ambient residential exposures to PM(10) was associated with a 4.3% (95% confidence interval [CI], 1.1-7.7%) increased risk of all-cause mortality. The increase for an IQR change in SO(2) was 6.9% (95% CI, 2.3-11.6%), for NO(2) was 8.2% (95% CI, 4.5-12.1%), and for PM(2.5) was 3.9% (95% CI, 1.0-6.9%). Elevated associations with cause-specific mortality (lung cancer, cardiovascular and respiratory disease) were observed for PM(2.5), SO(2), and NO(2), but not PM(10). None of the pollutants were confounded by occupational exposures. In multipollutant models, overall, the associations were attenuated, most strongly for PM(10). In sensitivity analyses excluding long-haul drivers, who spend days away from home, larger hazard ratios were observed.Conclusionsin this population of men, residential ambient air pollution exposures were associated with mortality.

Project description:BackgroundPlastic pollution is greatly serious in the ocean and soil. Microplastics (MPs) degraded from plastic has threatened animals and humans health. The accumulation of MPs in the tissues and blood in animals and humans has been found. There is therefore a need to assess the toxicological effects of MPs on the reproductive system.ResultsIn this study, we explored the effect of polystyrene microplastics (PS-MPs) on premature testicular aging in vitro and in vivo. In vitro, we found that testicular sertoli cells (TM4 cells) was prematurely senescent following PS-MPs treatment by the evaluation of a range of aging marker molecules (such as Sa-β-gal, p16 and 21). TM4 cells were then employed for in vitro model to study the potential molecular mechanism by which PS-MPs induce the premature senescence of TM4 cells. NF-κB is identified as a key molecule for PS-MPs-induced TM4 cellular senescence. Furthermore, through eliminating reactive oxygen species (ROS), the activation of nuclear factor kappa B (NF-κB) was blocked in PS-MPs-induced senescent TM4 cells, indicating that ROS triggers NF-κB activation. Next, we analyzed the causes of mitochondrial ROS (mtROS) accumulation induced by PS-MPs, and results showed that Ca2+ overload induced the accumulation of mtROS. Further, PS-MPs exposure inhibits mitophagy, leading to the continuous accumulation of senescent cells. In vivo, 8-week-old C57 mice were used as models to assess the effect of PS-MPs on premature testicular aging. The results illustrated that PS-MPs exposure causes premature aging of testicular tissue by testing aging markers. Additionally, PS-MPs led to oxidative stress and inflammatory response in the testicular tissue.ConclusionIn short, our experimental results revealed that PS-MPs-caused testicular premature aging is dependent on Ca2+/ROS/NF-κB signaling axis. The current study lays the foundation for further exploration of the effects of microplastics on testicular toxicology.

Dataset Information

Reaction of monocytes to polystyrene and silica nanoparticles in short-term and long-term exposures.

Publications

Reaction of monocytes to polystyrene and silica nanoparticles in short-term and long-term exposures.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets