Airborne Quinones Caused Cytotoxicity and DNA Damage in Human Vascular Endothelial Cells

Article Preview

Abstract:

Traffic-related particulate matter (PM) is found to be associated with adverse cardiovascular diseases. Quinones present in the traffic-related PM are hypothesized to contribute to these harmful effects through reactive oxygen species (ROS) generation. However, the impacts of the airborne quinones on the cytotoxic and genotoxic effects in human vascular endothelial cells are less well known. The aim of the present study is to assess whether exposure to three typical airborne quinones, including anthraquinone (AQ), 1,4-naphthroquinone (NQ) and benzoquinone (BQ), can induce cytotoxicity and DNA damage in the human umbilical vein endothelial cells (HUVEC). Cell viability, plasma membrane damage (lactate dehydrogenase leakage), and DNA damage were assessed in HUVEC after exposed to the three airborne quinones. Significant cytotoxicity was caused by the three quinones, indicating by the significant decrease in cell viability and significant increase in LDH activity. AQ and BQ slightly increased the DNA damage in HUVEC without significance. The ROS generation was not observed in HUVEC after exposed to AQ, NQ or BQ, suggesting that the cyototoxicity and the DNA damage caused by these quinones in HUVEC were not generated through the oxidative stress pathway. Our results suggest that AQ, NQ and BQ presented in the traffic-related particles may participate in the development of cardiovascular diseases through causing cytotoxicity and DNA damage in vascular endothelial cells.

You might also be interested in these eBooks

Info:

Periodical:

Advanced Materials Research (Volumes 610-613)

Pages:

681-685

Citation:

Online since:

December 2012

Export:

Price:

Permissions CCC:

Permissions PLS:

Сopyright:

© 2013 Trans Tech Publications Ltd. All Rights Reserved

Share:

Citation:

* - Corresponding Author

[1] K.A. Miller, D.S. Siscovick, L. Sheppard, K. Shepherd, J.H. Sullivan, G.L. Anderson, and J.D. Kaufman: N. Engl. J. Med. Vol. 356 (2007), p.447

Google Scholar

[2] S. Robertson, G.A. Gray, R. Duffin, S.G. McLean, C.A. Shaw, P.W.F. Hadoke, D.E. Newby and M.R. Miller: Part. Fibre Toxicol. Vol. 9 (2012), p.9

Google Scholar

[3] S.V. Roosbroeck, G. Hoek, K. Meliefste, N.A. Janssen, and B. Brunekreef: Environ. Sci. Technol. Vol. 42 (2008), p.1337

Google Scholar

[4] C. Walgraeve, K. Demeestere, J. Dewulf, R. Zimmermann, and H.V. Langenhove: Atmos. Environ. Vol. 44 (2010), p.1831

Google Scholar

[5] Y. Shang, C. Chen, Y. Li, J. C. Zhao, and T. Zhu: Environ. Sci. Technol. Vol. 46 (2012), p.2935

Google Scholar

[6] V. Klaus, T. Hartmann, J. Gambini, P. Graf, W. Stahl, A. Hartwig, and L.O. Klotz: Arch. Biochem. Biophys.Vol. 496 (2010), p.93

Google Scholar

[7] J. Oda, S. Nomura, A. Yasuhara, and T. Shibamoto: Atmos. Environ. Vol. 35 (2001), p.4819

Google Scholar

[8] A. Eiguren-Fernandez, A.H. Miguel, E. Di Stefano, D.A. Schmitz, A.K. Cho, S. Thurairatnam, and J.R. Froines: Aerosol. Sci. Technol. Vol. 42 (2008), p.854

DOI: 10.1080/02786820802339546

Google Scholar

[9] Y.J. Wei, I.K. Han, M. Hu, M. Shao, J.J. Zhang, X. Y. Tang: Chemosphere. Vol. 81 (2010), p.1280

Google Scholar

[10] I. Wakabayashi, K. Sakamoto, and K. Hatake: Pharmacol Toxicol Vol. 68 (1991), p.187

Google Scholar

[11] Y. Kumagai, T. Hayashi, T. Miyauchi, A. Endo, A. Iguchi, M. Kiriya-Sakai, S. Sakai, K. Yuki, M. Kikushima, and N. Shimojo: Am. J. Physiol. Regul. Integr. Comp. Physiol. Vol. 281 (2001), p. R25

DOI: 10.1152/ajpregu.2001.281.1.r25

Google Scholar

[12] M.J. Campen: Arch. Toxicol. Vol. 86 (2012), p.517

Google Scholar

[13] R.R. Tice, E. Agurell, D. Anderson, B. Burlinson, A. Hartmann, H. Kobayashi, Y. Miyamae, E. Rojas, J.-C. Ryu, and Y.F. Sasaki: Environ. Mol. Mutagen. Vol. 35 (2000), p.206

DOI: 10.1002/(sici)1098-2280(2000)35:3<206::aid-em8>3.0.co;2-j

Google Scholar