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Cyclobutane pyrimidine dimers (CPDs) are a form of DNA damage that is caused by UV exposure. CPDs interfere with base pairing during DNA replication – which can lead to mutations and cancer.
UVB radiation is directly absorbed by DNA. The energy causes changes in the bonding of pyrimidine structures found in DNA leading to CPDs and pyrimidine-pyrimidone (6-4) photoproducts.
UVA on the other hand is poorly absorbed by DNA, but was also found to cause CPD formation in human skin. CPDs were found to remain longer in the skin when there was UVA exposure, leading to speculation that UVA may also suppress a repair mechanism.
Our cells do have DNA repair capabilities, where damaged DNA is excised and replaced – but these processes can be overwhelmed by an accumulation of damage.
Experiments have measured the amount of CPD formation in human skin when exposed to UVB. One study found that CPDs were formed even when there was no visible sunburn (0.5 sunburn dose). They also found CPDs in both the epidermis and dermis and these levels were elevated for about 10 days as the skin sloughed off.
These two images from the paper show (A) skin that was not exposed to UVB and (B) skin that was exposed to UVB. The brown staining of the cells indicates presence of CPDs.
The amount of CPDs found in both the epidermis and dermis increased as UVB exposure increased.
A recent experiment performed by Pierre Fabre (manufacturers of Avène) looked at the effect sunscreen had on the formation of CPDs in human skin after UV exposure.
14 volunteers applied a sunscreen to their forearm and were exposed to UVB and UVA on skin protected by the sunscreen and also on unprotected skin. The area covered in sunscreen received 15 times the dose of UV to cause sunburn, whereas the unprotected skin received 2 times the dose.
After this exposure, their skin was blistered by vacuum and the contents of the blister were examined for CPDs using two different methods: immunostaining and spectrometry (HPLC-MS).
They found that the unprotected skin after exposure to UV had an elevated ratio of CPDs to normal DNA bases (90 CPD to 106 DNA bases). In comparison, the skin protected with the sunscreen had an amount of CPDs similar to unexposed skin and statistically significantly less than the unprotected skin (P < 0.001) – even though the area received more UV exposure. The CPD to normal DNA base ratio was not reported for the sunscreen protected and unexposed skin.
The sunscreen was not named, but it is SPF 50+, broad spectrum, and contained; Tinosorb M and S, Iscotrizinol, Avobenzone, and the antioxidant bis-ethylhexyl-hydroxydimethoxy benzylmalonate.
Preventing the formation of CPDs from reducing UV exposure is the most well-researched option, but there are other newer methods that are emerging – some of which are already available on the market.
Photolyase is a DNA repair enzyme that can be activated by the absorption of a photon and transfer an electron to the CPD, this can separate the CPD back into two normal pyrimidine bases – with the right timing. In humans, the photolyase enzyme no longer works, but there is some evidence that topical application of photolyase may reduce the formation of CPDs. An experiment where photolyase encapsulated in liposomes combined with light exposure was applied to human skin reduced the formation of CPDs by 40%-45% after exposure to UVB.
You can watch a lecture given by Aziz Sanzar about photolyase and DNA repair below. He won the Nobel Prize in Chemistry in 2015 for his work along with his colleagues Tomas Lindahl and Paul Modrich.
S.K. Katiyar, M.S. Matsui, H. Mukhtar, Kinetics of UV light–induced cyclobutane pyrimidine dimers in human skin in vivo: An immunohistochemical analysis of both epidermis and dermis, Photochemistry and Photobiology (2002), DOI: 10.1562/0031-8655(2000)0720788KOULIC2.0.CO2
J. Gwendal, T. Douki, J. Le Digabel, et al, Evaluation of the protection of a broad-spectrum SPF50+ sunscreen against DNA damage, Journal of the American Academy of Dermatology (2018), DOI: 10.1016/j.jaad.2018.05.570
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