Fluorescence intensity images of human skin corneocytes at 0 J m^-2 (a) and 550 J m^-2 (b), and granular (c) and spinous and basale keratinocytes (d) at 500 J m^-2. The fluorescence intensity of (a) is representative of all images regardless of depth. The intensity scale is given below each image. (Courtesy K. Hanson and R. Clegg)

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Supported by the National Institutes of Health, the Skin Cancer Foundation, the Cancer Research Foundation, and Roche Vitamins, Professor Robert Clegg and Dr. Kerry Hanson use two-photon fluorescence intensity imaging to study the sources of photodamage to human skin.Photodamage is cumulative, resulting from repetitive UV-induced photoreactions within the skin, which taken individually may seem trivial, but over the course of one's lifetime cause cumulative damage to the cells of the skin. Case in point: One sunburn in childhood may seem simply inconvenient and uncomfortable, but it dramatically increases our risk of skin cancer later in life. Concurrent with advances in technology has come an understanding that UV radiation also induces effects in the skin, such as immune suppression, lipid oxidation, and mitochondrial destruction, that are not detectable by eye following a day spent at the beach. 

And most worrisome, these effects, similar to tanning and sunburn, are responsible for photoaging, actinic keratosis, and/or skin cancers. Recent research shows that photodamage (wrinkles, immune suppression, skin cancers) occurs, in part, because of photoreactions involving reactive oxygen species (ROS) in the skin. Energetically excited derivatives of molecular oxygen, ROS include singlet oxygen (¹O₂), hydrogen peroxide (H₂O₂), superoxide (O₂^·-) and nitric oxide (NO), which react and destroy lipid membranes, induce inflammatory cytokines, and trigger apoptosis. In addition, more than 90 percent of the visible signs of aging are attributed to ROS-induced photodamage that accumulates over a lifetime. 

The Clegg group is interested in understanding how lightly pigmented skin responds to North American summer sun. A kinetic model has been developed to estimate the concentration of ROS that are generated within the facial skin of lightly pigmented individuals. Following UVB irradiation equivalent to only two hours of noonday summer North American solar exposure, approximately 10^-4 moles of ROS may be generated in the lower epidermal strata. Repeated exposure to UV will continue to generate more ROS, and up to 57 moles of ROS may be generated within the skin over the course of one's lifetime, increasing the risk of photoaging, immunomodulation, and skin cancers. 

More information about this exciting work and other experimental biophysics projects in the Laboratory for Fluorescence Dynamics is available from Professor Clegg or Dr. Hanson.

And don't forget the sunscreen!