Endogenous Antioxidant Photoprotection and Its Enhancement in Human Skin

Authored by: Maryam Afshar , Antony R. Young

CRC Handbook of Organic Photochemistry and Photobiology

Print publication date:  March  2012
Online publication date:  March  2012

Print ISBN: 9781439899335
eBook ISBN: 9781466561250
Adobe ISBN:

10.1201/b12252-61

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Abstract

Terrestrial solar ultraviolet radiation (UVR) is a major environmental hazard and is the cause of the majority of skin cancers, especially in sun-sensitive white-skinned people. There is considerable evidence that nonmelanoma skin cancers are due to UVR-induced DNA damage (Ziegler et al., 1994). UVR also causes photoaging. The effects of UVR on the skin, whether acute such as sunburn or long term, are caused by damage to target molecules. This can be done in two ways: (1) Direct absorption of UVR by the target molecule such as DNA or urocanic acid. In such cases, the target molecule is the chromophore. One of the most important types of DNA damage formed in this way is the cyclobutane pyrimidine dimer (CPD), which has been implicated in erythema, immunosuppression, mutagenesis, and skin cancer (Yarosh, 2004). Alternatively (2) the target molecule can be damaged indirectly when UVR is absorbed by another chromophore, which generates reactive oxygen species (ROS), such as the superoxide anion, hydrogen peroxide, the hydroxyl radical, and singlet oxygen. ROS can interact with cellular proteins, membranes, and DNA to alter their functions. Consequently, excessive ROS may arrest the cell growth cycle and cause inflammation, immunosuppression, skin aging, DNA damage (Cadet et al., 2009), mutation, and cancer.

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