Dataset Information

Ambient particulate matter (PM₁₀)-induced injury in feline lung cells and nutritional intervention.

ABSTRACT: Ambient particulate matter (APM) is extremely harmful to life's health. In this study, we investigated cellular injury in cat (Felix catus) lung cells (FCA-L2) exposed to organic and water-soluble extracts from APM. As well, the protective effect of vitamin E (VE), lycopene and a mixture of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (molar concentration ratio of 2:1) against this damage was evaluated. Organic and water-soluble extracts induced oxidative stress in FCA-L2 cells, as evidenced by excess reactive oxygen species production and mitochondrial damage, while treatment with VE, lycopene and EPA: DHA remarkably alleviated these indices. It was further found that treatment with EPA: DHA decreased lactate dehydrogenase and malondialdehyde, as well as increased activities of superoxide dismutase, glutathione peroxidase and catalase. Our study confirmed that nutrients mediates APM-induced oxidative stress via antioxidant proteins. Also, these findings could provide new insights into reducing APM-induced cytotoxicity by nutritional supplementation based on antioxidant compounds for animals.

SUBMITTER: Bai H

PROVIDER: S-EPMC9156945 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Ambient particulate matter (PM<sub>10</sub>)-induced injury in feline lung cells and nutritional intervention.

Bai Huasong H Wang Ying Y Wu Peng P Wang Zhanzhong Z

Heliyon 20220526 5

Ambient particulate matter (APM) is extremely harmful to life's health. In this study, we investigated cellular injury in cat (<i>Felix catus</i>) lung cells (FCA-L2) exposed to organic and water-soluble extracts from APM. As well, the protective effect of vitamin E (VE), lycopene and a mixture of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (molar concentration ratio of 2:1) against this damage was evaluated. Organic and water-soluble extracts induced oxidative stress in FCA-L2 ce ...[more]

PMID: 35663753

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Project description:The main objective of this study was chemical characterization and source apportionment of the oxidative potential of ambient PM2.5 samples collected in an urban background area in Athens, Greece. Ambient PM2.5 samples were collected during the summer (June-September) of 2017 and winter (February-March) of 2018 at a residential, urban background site in the outlying neighborhood of the Demokritos National Laboratory in Athens, Greece. The collected PM samples were analyzed for their chemical constituents including metals and trace elements, water-soluble organic carbon (WSOC), elemental and organic carbon (EC/OC), and marker of biomass burning (i.e., levoglucosan). In addition, the DCFH in vitro assay was performed to determine the oxidative potential of the PM2.5 samples. We performed a series of statistical analyses, including Spearman rank-order correlation analysis, principal component analysis (PCA), and multi linear regression (MLR) to determine the most significant species (as source tracers) contributing to the oxidative potential of PM2.5. Our findings revealed that the intrinsic (per PM mass) and extrinsic (per m3 of air volume) oxidative potentials of the collected ambient PM2.5 samples were significantly higher than those measured in many urban areas around the world. The results of the MLR analyses indicated that the major pollution sources contributing to the oxidative potential of ambient PM2.5 were vehicular emissions (characterized by EC) (44%), followed by secondary organic aerosol (SOA) formation (characterized by WSOC) (16%), and biomass burning (characterized by levoglucosan) (9%). The oxidative potential of the collected ambient PM2.5 samples was also higher in summer compared to the winter, mainly due to higher concentrations of EC and WSOC during this season. Results from this study corroborate the impact of traffic and SOA on the oxidative potential of ambient PM2.5 in greater Athens area, and can be helpful in adopting appropriate public health policies regarding detrimental outcomes of exposure to PM2.5.

Project description:Air pollution in megacities is increasing due to the dense population index, increasing vehicles, industries, and burning activities that negatively impact human health and climate. There is limited study of air pollution in many megacities of the world including Pakistan. Lahore is a megacity in Pakistan in which the continuous investigation of particulate matter is very important. Therefore, this study investigates particulate matter in three size fractions (PM1, PM2.5, and PM10) in Lahore, a polluted city in south Asia. The particulate matter was collected daily during the winter season of 2019. The average values of PM1, PM2.5, and PM10 were found to be 102.00 ± 64.03, 188.31 ± 49.21, and 279.73 ± 75.04 μg m-3, respectively. Various characterization techniques including X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), and scanning electron microscopy (SEM) combined with energy-dispersive X-ray spectroscopy (EDX) were used. FT-IR and XRD techniques identified the minerals and compounds like quartz, peroxides, calcites and vaterite, feldspar group, kaolinite clay minerals, chrysotile, vaterite, illite, hematite, dolomite, calcite, magnesium phosphate, ammonium sulfate, calcium iron oxide, gypsum, vermiculite, CuSO4, and FeSO4. Morphology and elemental composition indicated quartz, iron, biological particles, carbonate, and carbonaceous particles. In addition, various elements like C, O, B, Mg, Si, Ca, Cl, Al, Na, K, Zn, and S were identified. Based on the elemental composition and morphology, different particles along with their percentage were found like carbonaceous- (38%), biogenic- (14%), boron-rich particle- (14%), feldspar- (10%), quartz- (9%), calcium-rich particle- (5%), chlorine-rich particle- (5%), and iron-rich particle (5%)-based. The main sources of the particulate matter included vehicular exertion, biomass consumption, resuspended dust, biological emissions, activities from construction sites, and industrial emissions near the sampling area.

Project description:Exposure to atmospheric particulate matter (PM) is recognized as a human health risk factor of great concern. The present work aimed to study the cellular mechanisms underlying cytotoxic effects of airborne particulate matter <10 µm in size (PM10), sampled in an urban background site from January to May 2020, on A549 cells. In particular, the study addressed if PM10 exposure can be a main factor in the induction of the Apoptotic Volume Decrease (AVD), which is one of the first events of apoptosis, and if the generation of intracellular oxidative stress can be involved in the PM10 induction of apoptosis in A549 cells. The cytotoxicity of PM10 samples was measured by MTT test on cells exposed for 24 h to the PM10 aqueous extracts, cell volume changes were monitored by morphometric analysis of the cells, apoptosis appearance was detected by annexin V and the induction of intracellular oxidative stress was evaluated by the ROS sensitive CM-H2DCFDA fluorescent probe. The results showed cytotoxic effects ascribable to apoptotic death in A549 cells exposed for 24 h to aqueous extracts of airborne winter PM10 samples characterized by high PM10 value and organic carbon content. The detected reduced cell viability in winter samples ranged from 55% to 100%. Normotonic cell volume reduction (ranging from about 60% to 30% cell volume decrease) after PM10 exposure was already detectable after the first 30 min clearly indicating the ability of PM10, mainly arising from biomass burning, to induce Apoptotic Volume Decrease (AVD) in A549 cells. AVD was prevented by the pre-treatment with 0.5 mM SITS indicating the activation of Cl- efflux presumably through the activation of VRAC channels. The exposure of A549 cells to PM10 aqueous extracts was able to induce intracellular oxidative stress detected by using the ROS-sensitive probe CM-H2DCFDA. The PM10-induced oxidative stress was statistically significantly correlated with cell viability inhibition and with apoptotic cell shrinkage. It was already evident after 15 min exposure representing one of the first cellular effects caused by PM exposure. This result suggests the role of oxidative stress in the PM10 induction of AVD as one of the first steps in cytotoxicity.

Project description:BackgroundThe Metropolitan Area of São Paulo has a unique composition of atmospheric pollutants, and positive correlations between exposure and the risk of diseases and mortality have been observed. Here we assessed the effects of ambient fine particulate matter (PM2.5) on genotoxic and global DNA methylation and hydroxymethylation changes, as well as the activities of antioxidant enzymes, in tissues of AJ mice exposed whole body to ambient air enriched in PM2.5, which was concentrated in a chamber near an avenue of intense traffic in São Paulo City, Brazil.ResultsMice exposed to concentrated ambient PM2.5 (1 h daily, 3 months) were compared to in situ ambient air exposed mice as the study control. The concentrated PM2.5 exposed group presented increased levels of the oxidized nucleoside 8-oxo-7,8-dihydro-2'-deoxyguanosine in lung and kidney DNA and increased levels of the etheno adducts 1,N6-etheno-2'-deoxyadenosine and 1,N2-etheno-2'-deoxyguanosine in kidney and liver DNA, respectively. Apart from the genotoxic effects, the exposure to PM2.5 led to decreased levels of the epigenetic mark 5-hydroxymethylcytosine (5-hmC) in lung and liver DNA. Changes in lung, liver, and erythrocyte antioxidant enzyme activities were also observed. Decreased glutathione reductase and increased superoxide dismutase (SOD) activities were observed in the lungs, while the liver presented increased glutathione S-transferase and decreased SOD activities. An increase in SOD activity was also observed in erythrocytes. These changes are consistent with the induction of local and systemic oxidative stress.ConclusionsMice exposed daily to PM2.5 at a concentration that mimics 24-h exposure to the mean concentration found in ambient air presented, after 3 months, increased levels of DNA lesions related to the occurrence of oxidative stress in the lungs, liver, and kidney, in parallel to decreased global levels of 5-hmC in lung and liver DNA. Genetic and epigenetic alterations induced by pollutants may affect the genes committed to cell cycle control, apoptosis, and cell differentiation, increasing the chance of cancer development, which merits further investigation.

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Ambient particulate matter (PM₁₀)-induced injury in feline lung cells and nutritional intervention.

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Ambient particulate matter (PM<sub>10</sub>)-induced injury in feline lung cells and nutritional intervention.

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Dataset Information

Ambient particulate matter (PM10)-induced injury in feline lung cells and nutritional intervention.

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Ambient particulate matter (PM<sub>10</sub>)-induced injury in feline lung cells and nutritional intervention.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

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Ambient particulate matter (PM₁₀)-induced injury in feline lung cells and nutritional intervention.