Resveratrol-sensitized UVA induced apoptosis in human keratinocytes through mitochondrial oxidative stress and pore opening

Jean Z. Boyer, Jana Jandova, Jaroslav Janda, Frank R. Vleugels, David A. Elliott, James E Sligh

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Resveratrol (3,5,4'-trihydroxy-trans-stilbene), a polyphenol compound, is derived from natural products such as the skin of red grapes, blueberries and cranberries. Resveratrol not only exhibits antioxidant, cardioprotection, and anti-aging properties, but can also inhibit cancer cell growth and induce apoptosis. It has been shown that resveratrol inhibits the activation of Nf-κB and subsequently down regulates the expression of Nf-κB regulated genes such as interleukin-2 and Bcl-2, leading to cell cycle arrest and increased apoptosis in multiple myeloma cells. In the skin, resveratrol has been reported to sensitize keratinocytes to UVA induced apoptosis. However, the effect of resveratrol on opening of the mitochondrial permeability transition pore has not been previously examined. Our data show that UVA (14 J/cm 2) along with resveratrol causes massive oxidative stress in mitochondria. As a consequence of oxidative stress, the mitochondrial membrane potential decreases which results in opening of the mitochondrial pores ultimately leading to apoptosis in human keratinocytes. These results may have clinical implications for development of future chemotherapeutic treatment for tumors of the skin.

Original languageEnglish (US)
Pages (from-to)42-50
Number of pages9
JournalJournal of Photochemistry and Photobiology B: Biology
Volume113
DOIs
Publication statusPublished - Aug 1 2012

    Fingerprint

Keywords

  • Keratinocyte
  • Mitochondrial membrane potential
  • Mitochondrial permeability transition pore
  • Reactive oxygen species
  • Resveratrol
  • UVA induced apoptosis

ASJC Scopus subject areas

  • Radiation
  • Radiology Nuclear Medicine and imaging
  • Radiological and Ultrasound Technology
  • Biophysics

Cite this