Riboflavin Activated by UV Exposure Causes Oxidative DNA Damage, Which is Inhibited by Vitamin C

Gerd P. Pfeifer, Ph.D.
Beckman Research Institute
R37ES006070

NIEHS grantee Gerd Pfeifer and colleagues at the Beckman Research Institute report intriguing results of experiments involving the essential vitamin riboflavin. They found that riboflavin causes oxidative DNA damage when it is activated by ultraviolet radiation in a mouse fibroblast cell culture model. These effects were blocked when vitamin C was co-administered.

Pfeifer is one of only nine current Method to Extend Research In Time (MERIT) grantees at NIEHS. This is a prestigious award given only to very highly productive researchers who are leaders in their respective fields and have a history of good grantsmanship.

This work expands on a popular theory that wavelengths of light in the ultraviolet A (UVA) range trigger intracellular photosensitization reactions, leading to promutagenic oxidative DNA damage. Riboflavin, also known as vitamin B2, is known to be a cellular photosensitizer and was shown in the current studies to intensify the UVA-induced damage. However, vitamin C at a physiologic relevant dose exerted antioxidant effects and protected the cells from oxidative DNA damage. These findings confirm that UVA induced-genotoxicity is caused by intracellular photosensitization reactions, which generate oxidative and promutagenic damage to DNA.

Citation: Besaratinia A, Kim SI, Bates SE, Pfeifer GP. Riboflavin activated by ultraviolet A1 irradiation induces oxidative DNA damage-mediated mutations inhibited by vitamin C. Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):5953-8.