Sunburn solution: UV damage pivots on single electron

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  • Published: Aug 1, 2011
  • Author: David Bradley
  • Channels: UV/Vis Spectroscopy
thumbnail image: Sunburn solution: UV damage pivots on single electron

Life-saving examination

Scientists working for almost ten years on the puzzle of how UV-damaged DNA undergoes enzymatic repair work have at last observed the entire process in all its details in the laboratory. It seems that this life-saving process pivots on a single electron hinting at improved understanding of UV-induced skin cancer risk and perhaps novel treatments for sunburn.

Writing in the Proceedings of the National Academy of Sciences, researchers from Ohio State University and their colleagues at the University of North Carolina School of Medicine, Chapel Hill confirm what was already known about the enzyme photolyase: it is naturally produced in the cells of plants and some animals, but not by mammals, including humans. The enzyme fixes damaged DNA by tearing open the misshapen, damaged area of the DNA in two places and reforming it into its original, undamaged conformation.

Photolyase, it seems, does not make the two required breaks either side of the DNA injury at the same time. Instead, the process occurs in two steps one after the other. The first break occurs within a few trillionths of a second, the second break in 90-trillionths of a second. The breakups are separated because an energetic "messenger" electron is sent tunnelling its way along the outer edge of the damage site on a circuitous route through the DNA molecule from the first break point to the next in a dimeric photo lesion, specifically the ring-shaped cyclobutane pyrimidine dimer.


Taking the pulse of photolyase

According to team leader Dongping Zhong, the Robert Smith Professor of Physics and a professor in both the departments of chemistry and biochemistry at Ohio State University, they have now literally shed light on the repair process using a femtosecond pulsed laser to freeze the enzyme action, like strobe lighting in a nightclub freezes dancers. Zhong explains that the enzyme takes the "long way round" because this is actually the most efficient way for the electron to do its job.

"The enzyme needs to inject an electron into damaged DNA," he explains. "There are two pathways. One is the direct jump from the enzyme across the ring from one side to the other, which is a short distance. But instead the electron takes the scenic route. We found that along the way, there is another molecule that acts as a bridge to speed the electron flow, and in this way, the long route actually takes less time," Zhong adds.

With this knowledge in hand, the team hopes that other researchers might use the discovery to develop a kind of synthetic photolyase that could be used as an oral pharmaceutical or more likely a lotion to gently soothe sunburn and more effectively repair UV-damaged DNA. While insects, fish, birds, amphibians, marsupials, and even bacteria, viruses and yeast all benefit from photolyase, humans are susceptible to UV damaged to their DNA but do not have this particular repair enzyme. This could be especially important given the increasing numbers of fair-skinned people exposing themselves to strong sunlight on sunshine holidays closer to the Tropics and the apparent increase in skin cancer incidence associated with more UV exposure.



The views represented in this article are solely those of the author and do not necessarily represent those of John Wiley and Sons, Ltd.

 Scientists working for almost ten years on the puzzle of how UV-damaged DNA undergoes enzymatic repair work have at last observed the entire process in all its details in the laboratory; characterisation was carried out with femtosecond-resolved fluorescence dynamics and examination of the complete emission spectra of the system.

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