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Sun worshippers may someday slather on an after-suntan lotion that
repairs some of the genetic damage caused by ultraviolet (UV) light.
According to researchers in Germany and the Netherlands, a compound
under study that contains a DNA-repairing enzyme may allow sunburn
sufferers to reverse some skin-cell mutations that can later become
cancer.
The treatment reduced a key sign of skin damage by 40% to 45% among
19 study volunteers who were exposed to UVB radiation long enough
to get a mild burn.
The lotion could allow people to not only prevent burns with conventional
sunscreens, but to also perform damage control after burns occur.
Exposure to the sun's rays can harm DNA in skin cells, which can
lead to cancer. Such DNA mutations often include lesions called
pyrimidine dimers; researchers believe these lesions contribute
to cancer by damaging tumor-suppressing genes and by hindering the
immune system's response to sunburn.
The researchers took aim at dimers with a lotion containing a DNA-repairing
enzyme called photolyase. Found in many primitive organisms and
certain higher life forms such as fish, photolyase is activated
by light and specifically targets and removes pyrimidine dimers
from DNA.
Human skin has its own DNA-repair system, but whether it can sustain
such a light-activated photolyase response is still not certain,
Stege's team reports. The recent discovery of a human version of
a photolyase gene has "raised the possibility" that photolyase therapy
could help sun-damaged human skin, the researchers explain. The
current study looked at a lotion with photolyase derived from plankton.
After exposing the study participants to enough UVB exposure to
cause mild burns, the researchers found significant numbers of pyrimidine
dimers in their skin cells. Subjects were immediately treated with
the lotion, and one hour later were exposed to light waves in order
to activate the photolyase. Treatment cut skin-cell dimers by up
to 45%. In contrast, the researchers note, no reduction was seen
in additional experiments using lotion without photolyase or using
light therapy before applying the lotion.
By removing dimers from skin-cell DNA, the lotion also completely
prevented the suppression of two immune responses that help repair
sun damage, the investigators report. In untreated UVB-exposed skin,
however, these responses were inhibited.
Because these immune responses were protected by only partially
removing dimers from sun-damaged skin cells, it may not be necessary
to completely rid DNA of dimers for the treatment to work, the authors
note. They speculate that a certain number of dimers might have
to be present to override immune responses.
Proceedings of the National Academy
of Sciences February 15, 2000;97:1790-1795
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