Protection of Human Fibroblasts from Reactive Oxygen Species by Green Tea Polyphenolic Compounds

Article Preview

Abstract:

The potential protective roles played by green tea compounds (GTPCs) against reactive oxygen species-induced oxidative stress in cultured fetal human dermal fibroblasts (fHDFs) were investigated according to cell viability measurement methods, such as fluorescence double staining followed by flow cytometry (FCM), MTT assay and crystal violet uptake. Oxidative stress was induced in the fHDFs, either by adding 50 mM H2O2 or by the action of 40 U/L xanthine oxidase (XO) in the presence of xanthine (250 µM). FCM analysis was the most suitable to show that both treatments produced a significant (p < 0.05) reduction in the fHDF viability, attributed to its high sensitivity. On the microscopic observations, the cell death with necrotic morphology was appreciably induced by both treatments. These oxidative stress-induced damages were significantly (p < 0.05) prevented by pre-incubating the fHDFs with 200 µg/ml GTPC for 1 h. These results suggest that GTPC can act as a biological antioxidant in a cell culture experimental model and prevent oxidative stress-induced cytotoxicity in cells.

You might also be interested in these eBooks

Info:

Periodical:

Key Engineering Materials (Volumes 288-289)

Pages:

665-668

Citation:

Online since:

June 2005

Export:

Price:

Permissions CCC:

Permissions PLS:

Сopyright:

© 2005 Trans Tech Publications Ltd. All Rights Reserved

Share:

Citation:

[1] H. Sies: Oxidative Stress, Oxidants and Antioxidants. (Academic Press, New York 1991).

Google Scholar

[2] E.A. Decker: Nutr. Rev. Vol. 53 (1995), p.49.

Google Scholar

[3] C. Manna, P. Galletti, V. Cucciolla, et al: J. Nutr. Vol. 127 (1997), p.286.

Google Scholar

[4] S. -H. Hyon, D. -H. Kim: J Biotechnol Vol. 85 (2001), p.241.

Google Scholar

[5] M. Nakayama, K, Suzuki, M. Toda, et al: Antivir. Res. Vol. 21 (1993), p.289.

Google Scholar

[6] C.S. Yang and Z. -Y. Wang: J. Natl. Cancer Inst. Vol. 85 (1993), p.1038.

Google Scholar

[7] Y.H. Park, D. -W. Han, H. Suh, et al: Cell Biol. Toxicol. Vol. 19 (2003), p.325.

Google Scholar

[8] J. -C. Park, B.J. Park, H. Suh, B.Y. Park and D.K. Rah: Yonsei Med. J. Vol. 42 (2001), p.587.

Google Scholar

[9] M. Ishiyama, H. Tominaga, M. Shiga, et al: Biol. Pharm. Bull. Vol. 19 (1996), p.1518.

Google Scholar

[10] P.T. Thang, S. Patrick, L.S. Teik and C.S. Yung: Burns Vol. 27 (2001), p.319.

Google Scholar

[11] D. -W. Han, Y.H. Park, J.K. Kim, et al: J. Biotechnol. Vol. 110 (2004), p.109.

Google Scholar