scholarly journals A Toxicology Suite Adapted for Comparing Parallel Toxicity Responses of Model Human Lung Cells to Diesel Exhaust Particles and Their Extracts

2015 ◽  
Vol 49 (8) ◽  
pp. 599-610 ◽  
Author(s):  
Jane Turner ◽  
Mark Hernandez ◽  
John E. Snawder ◽  
Alina Handorean ◽  
Kevin M. McCabe
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Wei Zhang ◽  
Qifei Li ◽  
Mingjie Tang ◽  
Han Zhang ◽  
Xiaoping Sun ◽  
...  

AbstractDiesel exhaust particles (DEPs) are major air pollutants that lead to numerous human disorders, especially pulmonary diseases, partly through the induction of oxidative stress. Resveratrol is a polyphenol that ameliorates the production of reactive oxygen species (ROS) and delays aging-related processes. Herein we studied the cytoprotective effect of resveratrol on DEP-exposed human lung cells in a factorial experimental design. This work investigates biophysical features including cellular compositions and biomechanical properties, which were measured at the single-cell level using confocal Raman microspectroscopy (RM) and atomic force microscopy (AFM), respectively. Principal component analysis (PCA), hierarchical cluster analysis (HCA) and partial least square regression (PLS) analysis were applied to analyze Raman spectra with and without resveratrol protection. The health status of individual cells could be effectively predicted using an index derived from characteristic Raman spectral peak (e.g., 1006 cm−1) based on PLS model. AFM measurements indicated that cellular adhesion force was greatly reduced, while Young’s modulus was highly elevated in resveratrol treated DEP-exposed cells. Anti-oxidant resveratrol reduced DEP-induced ROS production and suppressed releases of several cytokines and chemokines. These findings suggest resveratrol may enhance resistance of human lung cells (e.g., SAEC) to air pollutants (e.g. DEPs).


1999 ◽  
Vol 27 (11-12) ◽  
pp. 1251-1258 ◽  
Author(s):  
Hiroshi Tokiwa ◽  
Nobuyuki Sera ◽  
Youichi Nakanishi ◽  
Masaru Sagai

2007 ◽  
Vol 101 (6) ◽  
pp. 1155-1162 ◽  
Author(s):  
G. Mazzarella ◽  
F. Ferraraccio ◽  
M.V. Prati ◽  
S. Annunziata ◽  
A. Bianco ◽  
...  

2009 ◽  
Vol 6 (1) ◽  
pp. 26 ◽  
Author(s):  
Andrea D Lehmann ◽  
Fabian Blank ◽  
Oliver Baum ◽  
Peter Gehr ◽  
Barbara M Rothen-Rutishauser

2015 ◽  
Vol 49 (14) ◽  
pp. 8721-8730 ◽  
Author(s):  
Linda C. Stoehr ◽  
Pierre Madl ◽  
Matthew S. P. Boyles ◽  
Roland Zauner ◽  
Monika Wimmer ◽  
...  

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 291
Author(s):  
Joong Won Lee ◽  
Hee Jae Lee ◽  
Young-Joo Lee ◽  
Yong-beom Lim ◽  
Woo Jong Sim ◽  
...  

Several epidemiological studies concluded that inhalation of diesel exhaust particles (DEP) is associated with an increase in the relative risk of lung cancer. In vitro research evaluating the genetic damage and/or changes in gene expression have been attempted to explain the relationship between DEP exposure and carcinogenicity. However, to date, investigations have been largely confined to studies in immortalized or tumorigenic epithelial cell models. Few studies have investigated damage at the chromosomal level to DEP exposure in normal cell lines. Here, we present the genotoxic effects of DEP in normal cells (embryonic human lung fibroblasts) by conventional genotoxicity testing (micronuclei (MN) and comet assay). We show the differentially expressed genes and enriched pathways in DEP-exposed WI-38 cells using RNA sequencing data. We observed a significant increase in single-strand DNA breaks and the frequency of MN in DEP-exposed cells in a dose-dependent manner. The differentially expressed genes following DEP exposure were significantly enriched in the pathway for responding to xenobiotics and DNA damage. Taken together, these results show that DEP exposure induced DNA damage at the chromosomal level in normal human lung cells and provide information on the expression of genes associated with genotoxic stress.


2013 ◽  
Vol 81 ◽  
pp. 380-388 ◽  
Author(s):  
Sandro Steiner ◽  
Jan Czerwinski ◽  
Pierre Comte ◽  
Olga Popovicheva ◽  
Elena Kireeva ◽  
...  

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