Caffeine protects human skin fibroblasts from acute reactive oxygen species-induced necrosis.

Abstract

Oxidative damage by reactive oxygen species (ROS) plays a major role in aging and carcinogenesis. Little is known about either the effects of acute ROS in necrosis and inflammation of skin or the therapeutic agents for prevention and treatment. Previously, our laboratory identified caffeine as an inhibitor of hydrogen peroxide (H2O2)-generated lipid peroxidation products in human skin fibroblasts. Here, we study effects of caffeine on acute ROS-mediated necrosis. Human skin fibroblasts were incubated with caffeine, followed by H2O2 challenge. Flow cytometry was used to analyze cell morphology, counts, apoptosis and necrosis, and ROS. We found that caffeine protects from H2O2 cell damage at lower (0.01 mM) and intermediate (0.1 mM) doses. The beneficial effects of caffeine appear to be mediated by a mechanism other than antioxidant function.

• Authors: Jonathan I Silverberg, Mital Patel, Neil Brody, Jared Jagdeo
• Journal: Journal of drugs in dermatology : JDD (J Drugs Dermatol) Vol. 11 Issue 11 Pg. 1342-6 (Nov 2012) ISSN: 1545-9616 [Print] United States
• PMID: 23135086 (Publication Type: Journal Article)

Chemical References

• Reactive Oxygen Species
• Caffeine
• Hydrogen Peroxide

Topics

• Apoptosis (drug effects)
• Caffeine (administration & dosage, pharmacology)
• Cells, Cultured
• Dose-Response Relationship, Drug
• Fibroblasts (drug effects, metabolism)
• Flow Cytometry
• Humans
• Hydrogen Peroxide (toxicity)
• Necrosis (prevention & control)
• Oxidative Stress (drug effects)
• Reactive Oxygen Species (metabolism)