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. 2016 Dec 14;9(1):e1267077. doi: 10.1080/19381980.2016.1267077

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© 2017 The Author(s). Published with license by Taylor & Francis

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 4. — The consequences of DNA photoproduct damage from exposure to outdoor UVA and UVB radiation versus indoor UVA radiation. Outdoor sunshine has both UVA and UVB radiation vs. indoor sunshine that has only UVA radiation because, unlike UVB, it can pass through window glass. The outdoor UVB radiation causes efficient pyrimidine dimer formation and UVA makes benzothiazine or benzothiazinylalanine and other radicals (λ_max >340 nm) that cannot react with the pyrimidine dimers formed outdoors because the covalent bonds block the available reaction sites (competitive reaction); whereas, indoor UVA forms few dimers so that many pyrimidine sites are available to react with the benzothiazine radicals it forms. Besides UVA creating ROS that oxidizes deoxyguanosine to 8-oxodG (G = O in diagram), UVA can create ONOO- radicals that can also make CPD in the dark for several hours post exposure [80].