Ultrastructural Changes in Cultured Rat Alveolar Macrophage Cells Induced by Fine Particulate Matter

Article Preview

Abstract:

Numerous studies have reported the association between fine particle matter (PM) and lung diseases. Alveolar macrophages (AM) are the key lung cells with strong capability of eliminating external particle pollutant. Therefore the prevention of AM from apoptosis induced by fine PM is vital for clinical treatment of increased pulmonary diseases. This study aims to investigate the ultrastructural changes in cultured AM induced by fine PM, which can directly reflect the effect of fine PM on AM apoptosis. In addition, Standard Reference Material for fine PM (SRM 2786) was used in current study due to its relative uniform composition. The results in this study suggested that SRM 2786 induced morphology changes in AM in a dose-dependent manner by transmission electron microscope observation, including nuclear fragmentation, chromatin aggregation, increased numbers of lysosomes and so forth. Consequently, this study provides reliable evidence for us to further investigate the apoptotic mechanism of AM induced by fine PM treatment in the future.

You might also be interested in these eBooks

Info:

Periodical:

Advanced Materials Research (Volumes 998-999)

Pages:

354-357

Citation:

Online since:

July 2014

Export:

Price:

Permissions CCC:

Permissions PLS:

Сopyright:

© 2014 Trans Tech Publications Ltd. All Rights Reserved

Share:

Citation:

* - Corresponding Author

[1] Elinkova J and Branis M. Int Arch Occup Environ Health. Vol. 74 (2001): p.565–573.

Google Scholar

[2] Bell ML and Davis DL. Environ Health Perspect. Vol. 109 (2001): p.389–394.

Google Scholar

[3] Schwartz, J. Epidemiology. Vol. 7 (1996): p.20 –28.

Google Scholar

[4] Hogg JC and Eeden SV. Respirology. Vol. 14 (2009): p.336–346.

Google Scholar

[5] Becker S, Soukup JM and Devlin RB. Toxicol Appl Pharmacol. Vol. 141 (1996): p.637–648.

Google Scholar

[6] Tiwari S, Srivastava AK and Padmanabhamuty B. J Atmos Chem. Vol. 62 (2009): pp.193-209.

Google Scholar

[7] Mitkus RJ, Powell J and Squibb KS. Toxicol In Vitro. Vol. 27 (2013): pp.2289-2298.

Google Scholar

[8] Kerr JFR, Wyllie AH and Currie AR. Br J Cancer. Vol. 26 (1972): pp.239-257.

Google Scholar

[9] Smith KR, Veranth JM and Aust AE. Chem Res Toxicol. Vol. 13 (2000): p.118–125.

Google Scholar

[10] Li N, Hao M and Nel AE. Clin Immunol. Vol. 109 (2003): p.250–265.

Google Scholar

[11] Gualtieri M, øvrevik J and Holme JA. Mutat Res-fund Mol M. 713 (2011): pp.18-31.

Google Scholar

[12] Guicciardi ME, Leist M and Gores GJ. Oncogene. Vol 23 (2004): pp.2881-2890.

DOI: 10.1038/sj.onc.1207512

Google Scholar

[13] Gavrieli Y, Sherman Y and Ben-Sasson SA. J Cell Biol. Vol. 119 (1992): pp.493-501.

Google Scholar