Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Photochem Photobiol B. 2009 Jun 3;95(3):196-203. doi: 10.1016/j.jphotobiol.2009.03.007. Epub 2009 Mar 29.

Caffeic acid modulates ultraviolet radiation-B induced oxidative damage in human blood lymphocytes.

Author information

  • 1Department of Biochemistry and Biotechnology, Annamalai University, Tamilnadu, India. drprasadnr@gmail.com

Abstract

Ultraviolet (UV) radiation causes inflammation, gene mutation and immunosuppressin in the human skin cells. These biological changes are responsible for photocarcinogenesis and photoaging. Normal lymphocytes are highly sensitive to the damaging effect of UV-radiation and undergo cell death. In the present study, the photoprotective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in the UVB (280-320) irradiated human blood lymphocytes. Lymphocytes pretreated with increasing concentration of caffeic acid (l, 5 and 10 microg/mL) for 30min were irradiated and lipid peroxidation, antioxidant defence status, cell viability (by MTT assay) and DNA damage (by comet assay) were examined. UVB-irradiation causes increased levels of lipid peroxidation, DNA damage and decreased antioxidant status, cell viability in human lymphocytes. Caffeic acid pretreatment significantly reduced the levels of lipid peroxidation markers i.e. thiobarbituric acid reactive substance (TBARS), lipid hydroperoxide (LPH), conjugated diene (CD) and decreased DNA damage (tail length and % tail DNA) in UVB-irradiated lymphocytes. Further, caffeic acid pretreatment significantly maintains antioxidant status and decreased UVB-induced cytotoxicity. The maximum dose of caffeic acid (l0 microg/mL) normalized the UVB induced cellular changes indicating the photoprotective effect of caffeic acid in irradiated lymphocytes.

PMID:
19386510
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk