Reactive oxygen species production and inflammatory effects of ambient PM2.5 -associated metals on human lung epithelial A549 cells “one year-long study”: The Delhi chapter

Das, Ananya; Habib, Gazala; Vivekanandan, Perumal; Kumar, Arun

doi:10.1016/j.chemosphere.2020.128305

Cited by 35 publications

(22 citation statements)

References 123 publications

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“…S1 ). This effect dose was similar to reports in which the dose of SRM 1648a to reduce cell viability to 50% was about 500 μg/mL [ 21 ]. Considering that previous studies have also shown that the optimum doses of PM2.5 to induce apoptosis, inflammatory cytokine release, or DNA damage in cells were between 200 to 500 μg/mL [ 22 – 26 ].…”

Section: Methodssupporting

confidence: 88%

PM2.5 promotes NSCLC carcinogenesis through translationally and transcriptionally activating DLAT-mediated glycolysis reprograming

Chen

Wang

Yang

et al. 2022

J Exp Clin Cancer Res

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Background Airborne fine particulate matter (PM2.5) has been associated with lung cancer development and progression in never smokers. However, the molecular mechanisms underlying PM2.5-induced lung cancer remain largely unknown. The aim of this study was to explore the mechanisms by which PM2.5 regulated the carcinogenesis of non-small cell lung cancer (NSCLC). Methods Paralleled ribosome sequencing (Ribo-seq) and RNA sequencing (RNA-seq) were performed to identify PM2.5-associated genes for further study. Quantitative real time-PCR (qRT-PCR), Western blot, and immunohistochemistry (IHC) were used to determine mRNA and protein expression levels in tissues and cells. The biological roles of PM2.5 and PM2.5-dysregulated gene were assessed by gain- and loss-of-function experiments, biochemical analyses, and Seahorse XF glycolysis stress assays. Human tissue microarray analysis and 18F-FDG PET/CT scans in patients with NSCLC were used to verify the experimental findings. Polysome fractionation experiments, chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assay were implemented to explore the molecular mechanisms. Results We found that PM2.5 induced a translation shift towards glycolysis pathway genes and increased glycolysis metabolism, as evidenced by increased L-lactate and pyruvate concentrations or higher extracellular acidification rate (ECAR) in vitro and in vivo. Particularly, PM2.5 enhanced the expression of glycolytic gene DLAT, which promoted glycolysis but suppressed acetyl-CoA production and enhanced the malignancy of NSCLC cells. Clinically, high expression of DLAT was positively associated with tumor size, poorer prognosis, and SUVmax values of 18F-FDG-PET/CT scans in patients with NSCLC. Mechanistically, PM2.5 activated eIF4E, consequently up-regulating the expression level of DLAT in polysomes. PM2.5 also stimulated transcription factor Sp1, which further augmented transcription activity of DLAT promoter. Conclusions This study demonstrated that PM2.5-activated overexpression of DLAT and enhancement in glycolysis metabolism contributed to the tumorigenesis of NSCLC, suggesting that DLAT-associated pathway may be a therapeutic target for NSCLC.

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Section: Methodssupporting

confidence: 88%

PM2.5 promotes NSCLC carcinogenesis through translationally and transcriptionally activating DLAT-mediated glycolysis reprograming

Chen

Wang

Yang

et al. 2022

J Exp Clin Cancer Res

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“…Oxidative stress is a consequence of the excessive ROS activity generated while antioxidant defenses are suppressed [59]. Numerous reports have demonstrated that oxidative stress plays an important role in the cytotoxicity, inflammatory response, and carcinogenesis of the PM-induced cells [58,[60][61][62]. The studies have shown that PM exposure increases intracellular ROS generation in human umbilical vein vascular endothelial cells [63], human microvascular endothelial cells [64], and human adenocarcinoma A549 cells [65].…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effects of Rosmarinic Acid Rich Fraction from Perilla on Oxidative Stress, Inflammation and Metastasis Ability in A549 Cells Exposed to PM via C-Jun, P-65-Nf-Κb and Akt Signaling Pathways

et al. 2021

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Particulate matter from forest fires (PMFF) is an environmental pollutant causing oxidative stress, inflammation, and cancer cell metastasis due to the presence of polycyclic aromatic hydrocarbons (PAHs). Perilla seed meal contains high levels of polyphenols, including rosmarinic acid (RA). The aim of this study is to determine the anti-oxidative stress, anti-inflammation, and anti-metastasis actions of rosmarinic acid rich fraction (RA-RF) from perilla seed meal and its underlying molecular mechanisms in A549 cells exposed to PMFF. PMFF samples were collected via the air sampler at the University of Phayao, Thailand, and their PAH content were analyzed using GC-MS. Fifteen PAH compounds were detected in PMFF. The PMFF significantly induced intracellular reactive oxygen species (ROS) production, the mRNA expression of pro-inflammatory cytokines, MMP-9 activity, invasion, migration, the overexpression of c-Jun and p-65-NF-κB, and Akt phosphorylation. Additionally, the RA-RF significantly reduced ROS production, IL-6, IL-8, TNF-α, and COX-2. RA-RF could also suppress MMP-9 activity, migration, invasion, and the phosphorylation activity of c-Jun, p-65-NF-κB, and Akt. Our findings revealed that RA-RF has antioxidant, anti-inflammatory, and anti-metastasis properties via c-Jun, p-65-NF-κB, and Akt signaling pathways. RA-RF may be further developed as an inhalation agent for the prevention of lung inflammation and cancer metastasis induced by PM exposure.

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“…This is consistent with the results of several studies. A seasonal toxicology study conducted in Delhi, India, revealed that cells exposed to PM in winter had higher levels of IL-6 compared with such levels in all other seasons, indicating that PM toxicity in winter was exacerbated by the burning of recrackers and open agricultural res [43]. In addition, a study in Milan reported that winter PM 2.5 , which was mostly contributed by fuel combustion, caused an increase in the IL-6 synthesis of human bronchial epithelial BEAS-2B cells after 24 h exposure [44].…”

Section: Discussionmentioning

confidence: 99%

Effects of domestic solid fuel combustion emissions on the biomarkers of homemakers in rural areas of the Fenwei Plain, China

Rong

et al. 2021

Preprint

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Background The health effects of heavy solid fuel use in winter in rural China are of concern. The effects of air pollution resulting from domestic solid fuel combustion in rural households on rural homemakers’ biomarkers were revealed in this study. Methods In total, 75 female homemakers from rural areas of Guanzhong Basin, the Fenwei Plain, People’s Republic of China, were randomly selected and divided into three groups (biomass users, coal users, and nonusers of solid fuel user [control group]). The differences in biological indicators, including 8-hydrox-2’-deoxyguanosine (8-OHdG), interlukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) in urine samples as well as blood pressure (BP, including systolic BP [SBP] and diastolic BP [DBP]) and heart rate (HR) among the groups in winter and summer were investigated using statistical analysis. Results IL-6, 8-OHdG, HR, SBP, and DBP were significantly higher in winter than in summer (P < 0.05) owing to the poor air quality resulted from the excessive use of solid fuels in winter. Significant seasonal differences in 8-OHdG, HR, and SBP were observed for both coal and biomass users. After the influence of confounders was removed, only IL-6 levels in the urine of solid fuel users were significantly higher than that of the control group. Conclusions IL-6 is a sensitive biomarker representing inflammatory responses to particulate matter emitted through household solid fuel combustion. Locally, excessive use of solid fuels in winter posed serious PM2.5 pollution in this area and adverse effects on inflammatory biomarkers in these rural homemakers and induced DNA damage related to oxidative stress.

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Reactive oxygen species production and inflammatory effects of ambient PM2.5 -associated metals on human lung epithelial A549 cells “one year-long study”: The Delhi chapter

Cited by 35 publications

References 123 publications

PM2.5 promotes NSCLC carcinogenesis through translationally and transcriptionally activating DLAT-mediated glycolysis reprograming

PM2.5 promotes NSCLC carcinogenesis through translationally and transcriptionally activating DLAT-mediated glycolysis reprograming

Suppressive Effects of Rosmarinic Acid Rich Fraction from Perilla on Oxidative Stress, Inflammation and Metastasis Ability in A549 Cells Exposed to PM via C-Jun, P-65-Nf-Κb and Akt Signaling Pathways

Effects of domestic solid fuel combustion emissions on the biomarkers of homemakers in rural areas of the Fenwei Plain, China

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