Literature DB >> 31751125

Exposure to Dimethyl Selenide (DMSe)-Derived Secondary Organic Aerosol Alters Transcriptomic Profiles in Human Airway Epithelial Cells.

C M Sabbir Ahmed, Yumeng Cui, Alexander L Frie, Abigail Burr, Rohan Kamath, Jin Y Chen, Arafat Rahman, Tara M Nordgren, Ying-Hsuan Lin, Roya Bahreini.   

Abstract

Dimethyl selenide (DMSe) is one of the major volatile organoselenium compounds released from aquatic and terrestrial environments through microbial transformation and plant metabolism. The detailed processes of DMSe leading to secondary organic aerosol (SOA) formation and the pulmonary health effects induced by inhalation of DMSe-derived SOA remain largely unknown. In this study, we characterized the chemical composition and formation yields of SOA produced from the oxidation of DMSe with OH radicals and O3 in controlled chamber experiments. Further, we profiled the transcriptome-wide gene expression changes in human airway epithelial cells (BEAS-2B) after exposure to DMSe-derived SOA. Our analyses indicated a significantly higher SOA yield resulting from the OH-initiated oxidation of DMSe. The oxidative potential of DMSe-derived SOA, as measured by the dithiothreitol (DTT) assay, suggested the presence of oxidizing moieties in DMSe-derived SOA at levels higher than typical ambient aerosols. Utilizing RNA sequencing (RNA-Seq) techniques, gene expression profiling followed by pathway enrichment analysis revealed several major biological pathways perturbed by DMSe-derived SOA, including elevated genotoxicity, DNA damage, and p53-mediated stress responses, as well as downregulated cholesterol biosynthesis, glycolysis, and interleukin IL-4/IL-13 signaling. This study highlights the significance of DMSe-derived SOA as a stressor in human airway epithelial cells.

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Year:  2019        PMID: 31751125      PMCID: PMC7458365          DOI: 10.1021/acs.est.9b04376

Source DB:  PubMed          Journal:  Environ Sci Technol        ISSN: 0013-936X            Impact factor:   9.028


  59 in total

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5.  Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis.

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  1 in total

1.  Lung Inflammatory Response to Environmental Dust Exposure in Mice Suggests a Link to Regional Respiratory Disease Risk.

Authors:  Abigail C Burr; Jalene V Velazquez; Arzu Ulu; Rohan Kamath; Sang Yong Kim; Amanpreet K Bilg; Aileen Najera; Iman Sultan; Jon K Botthoff; Emma Aronson; Meera G Nair; Tara M Nordgren
Journal:  J Inflamm Res       Date:  2021-08-21
  1 in total

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