ANN ARBOR---That golden tan may look terrific, but its cost to your skin---premature aging, wrinkles, sags, blotches, and an increased risk of skin cancer---may be more than you want to pay. While it is well known that ultraviolet radiation from the sun has many effects on skin, scientists still don't fully understand how UV causes so much damage.
University of Michigan scientists have discovered an important new piece of the puzzle, however, which they describe in an article to be published in this week's Nature Medicine.
"We found that ultraviolet irradiation blocks the ability of skin cells to recognize and respond to an essential nutrient called retinoic acid, which skin cells make from vitamin A or retinol," said John J. Voorhees, M.D., the Duncan and Ella Poth Distinguished Professor of Dermatology in the U-M Medical School. "The inability to respond to retinoic acid triggers a cascade of biochemical changes that upsets the normal balance between healthy and dying skin cells. In essence, UV causes a functional vitamin A deficiency in human skin.
"We also found that pretreating skin with retinoic acid---the active form of vitamin A---before UV exposure limits the extent of the harmful biochemical changes."
According to Gary J. Fisher, Ph.D., U-M senior associate research scientist in dermatology and the study's co-author, UV causes a major loss of retinoic acid receptors found in human skin cells. "Retinoic acid receptors are the molecular mediators of the biological actions of vitamin A. When retinoic acid receptors are lost, it is as if the skin has no vitamin A," Fisher explained. "This is a bad situation because vitamin A is required for normal skin development and function. Retinoic acid receptors, when activated by retinoic acid, transfer genetic instructions from DNA to the cell's protein-producing factory telling it to assemble proteins needed for skin cell function.
"Eight hours after skin was exposed to UV radiation in o
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Contact: Sally Pobojewski
pobo@umich.edu
734-647-1844
University of Michigan
30-Mar-1999