scholarly journals TiO2 nanoparticles generate superoxide and alter gene expression in human lung cells

RSC Advances ◽  
2019 ◽  
Vol 9 (43) ◽  
pp. 25039-25047 ◽  
Author(s):  
Dhanya T. Jayaram ◽  
Ashwath Kumar ◽  
Linda E. Kippner ◽  
Po-Yi Ho ◽  
Melissa L. Kemp ◽  
...  

Human lung cells have a multi-generational response to TiO2 nanoparticle exposure determined by RNA-Seq and fluorescence microscopy.

Virology ◽  
2006 ◽  
Vol 350 (2) ◽  
pp. 418-428 ◽  
Author(s):  
Xiao-Mei Rao ◽  
Xinyu Zheng ◽  
Sabine Waigel ◽  
Wolfgang Zacharias ◽  
Kelly M. McMasters ◽  
...  

RSC Advances ◽  
2020 ◽  
Vol 10 (72) ◽  
pp. 43950-43959
Author(s):  
Ozge Kose ◽  
Marion Stalet ◽  
Lara Leclerc ◽  
Valérie Forest

Characterization of the formation of the protein corona of TiO2 nanoparticles as a function of the main nanoparticle properties and investigation of potential relationship with the cytotoxicity nanoparticles induce in vitro in human lung cells.


2006 ◽  
Vol 1091 (1) ◽  
pp. 170-183 ◽  
Author(s):  
ANDREA ARENZ ◽  
CHRISTINE E. HELLWEG ◽  
NEVENA STOJICIC ◽  
CHRISTA BAUMSTARK-KHAN ◽  
HORST-HENNING GROTHEER

2016 ◽  
Vol 16 (22) ◽  
pp. 14079-14090 ◽  
Author(s):  
Maiko Arashiro ◽  
Ying-Hsuan Lin ◽  
Kenneth G. Sexton ◽  
Zhenfa Zhang ◽  
Ilona Jaspers ◽  
...  

Abstract. Atmospheric oxidation of isoprene, the most abundant non-methane hydrocarbon emitted into Earth's atmosphere primarily from terrestrial vegetation, is now recognized as a major contributor to the global secondary organic aerosol (SOA) burden. Anthropogenic pollutants significantly enhance isoprene SOA formation through acid-catalyzed heterogeneous chemistry of epoxide products. Since isoprene SOA formation as a source of fine aerosol is a relatively recent discovery, research is lacking on evaluating its potential adverse effects on human health. The objective of this study was to examine the effect of isoprene-derived SOA on inflammation-associated gene expression in human lung cells using a direct deposition exposure method. We assessed altered expression of inflammation-related genes in human bronchial epithelial cells (BEAS-2B) exposed to isoprene-derived SOA generated in an outdoor chamber facility. Measurements of gene expression of known inflammatory biomarkers interleukin 8 (IL-8) and cyclooxygenase 2 (COX-2) in exposed cells, together with complementary chemical measurements, showed that a dose of 0.067 µg cm−2 of SOA from isoprene photooxidation leads to statistically significant increases in IL-8 and COX-2 mRNA levels. Resuspension exposures using aerosol filter extracts corroborated these findings, supporting the conclusion that isoprene-derived SOA constituents induce the observed changes in mRNA levels. The present study is an attempt to examine the early biological responses of isoprene SOA exposure in human lung cells.


Metallomics ◽  
2012 ◽  
Vol 4 (8) ◽  
pp. 784 ◽  
Author(s):  
Hailey A. Clancy ◽  
Hong Sun ◽  
Lisa Passantino ◽  
Thomas Kluz ◽  
Alexandra Muñoz ◽  
...  

BMC Genomics ◽  
2007 ◽  
Vol 8 (1) ◽  
pp. 147 ◽  
Author(s):  
Veronique Malard ◽  
Frederic Berenguer ◽  
Odette Prat ◽  
Sylvie Ruat ◽  
Gerard Steinmetz ◽  
...  

Nanomaterials ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 649 ◽  
Author(s):  
Anda R. Gliga ◽  
Sebastiano Di Bucchianico ◽  
Emma Åkerlund ◽  
Hanna L. Karlsson

Production of nickel (Ni) and nickel oxide (NiO) nanoparticles (NPs) leads to a risk of exposure and subsequent health effects. Understanding the toxicological effects and underlying mechanisms using relevant in vitro methods is, therefore, needed. The aim of this study is to explore changes in gene expression using RNA sequencing following long term (six weeks) low dose (0.5 µg Ni/mL) exposure of human lung cells (BEAS-2B) to Ni and NiO NPs as well as soluble NiCl2. Genotoxicity and cell transformation as well as cellular dose of Ni are also analyzed. Exposure to NiCl2 resulted in the largest number of differentially expressed genes (197), despite limited uptake, suggesting a major role of extracellular receptors and downstream signaling. Gene expression changes for all Ni exposures included genes coding for calcium-binding proteins (S100A14 and S100A2) as well as TIMP3, CCND2, EPCAM, IL4R and DDIT4. Several top enriched pathways for NiCl2 were defined by upregulation of, e.g., interleukin-1A and -1B, as well as Vascular Endothelial Growth Factor A (VEGFA). All Ni exposures caused DNA strand breaks (comet assay), whereas no induction of micronuclei was observed. Taken together, this study provides an insight into Ni-induced toxicity and mechanisms occurring at lower and more realistic exposure levels.


2017 ◽  
Vol 51 (14) ◽  
pp. 8166-8175 ◽  
Author(s):  
Ying-Hsuan Lin ◽  
Maiko Arashiro ◽  
Phillip W. Clapp ◽  
Tianqu Cui ◽  
Kenneth G. Sexton ◽  
...  

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