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Editor’s note: Our regular columnist Mindy Goldstein, PhD, welcomes the following “Tech Edge” contribution from colleagues Alan M. Walfield and Daniel B. Yarosh.
From the column editor: It has been known for many years that continued sun exposure (UV radiation) leads to skin damage. The damage done by UV radiation is manifested in a number of ways including, cyclobutane pyrimidine dimers found in the DNA and oxidative damage to the DNA, proteins and lipids of the skin. Much of this damage is repaired by internal enzymes; however, some damage escapes repair and accumulates over time, resulting in accelerated skin aging, also known as photoaging. This month, I welcome Daniel B. Yarosh, PhD, from AGI Drmatics to present data on one aspect of DNA repair and photoaging. Yarosh is president and chairman of the board at AGI Dermatics, Located in Freeport,New York. Yarosh received his his doctorate in molecular biology from the University of Arizona College of Medicine in Tucson, Arizona, in 1978. He served as a National Science Foundation fellow at Brookhaven National Laboratory in Upton, New York, and then a staff fellow and cancer expert at the National Cancer Institute of the National Institutes of Health in Bethesda, Maryland. In 1985, Dr. Yarosh founded AGI Dermatics, where he placed an emphasis on the commercial application of DNA repair. Yarosh is the author of more than 100 scientific papers and two dozen patents and serves on the boards of the Photomedicine Society and the New York Biotechnology Association. In 2004, the International Union of Photobiology presented Yarosh with the Finsen Award, which is granted every four years at the International Congress for Photobiology for breakthrough research in the photobiology sciences.
The effects of photo-aging, as manifested by wrinkling, are produced by chronic exposure to solar ultraviolet (UV) radiation. UV irradiation also causes DNA damage. Not only does DNA damage increase the long-term risk for cancer, but it also increases the risk for photoaging through cytokine signaling between the keratinocytes and fibroblasts of the epidermis and dermis. These cytokines then elicit stress responses such as the secretion of matrix metalloproteinase-1 (MMP-1) into the dermis, leading to the degradation of collagen and wrinkling. It is shown that the delivery of DNA repair enzymes using liposomes provides protection from DNA damage in vitro and in vivo, reduction in MMP-1 responses as a marker for photo-aging and lessened wrinkling in a clinical trial.
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