UV-RADIATION DEPLETES ANTIOXIDANTS AND CAUSES OXIDATIVE DAMAGE IN A MODEL OF HUMAN SKIN

The degree to which antioxidant loss occurs in human skin after UV irr adiation is unknown, as is the cascade of events that might occur. We have, therefore, evaluated a tissue culture model of human skin for it s usefulness for studying oxidative injury by UV-irradiation. Human sk in equivalents, a tissue culture model, were irradiated using a full s olar UV spectrum (UVA and UVB, 280-400 nm) (0 to 16.8 J/cm(2), 0-12 mi nimal erythemal dose, MED), then incubated from 1 to 24 h. Ubiquinol w as the most UV-light sensitive antioxidant and was depleted by 2.1 J/c m(2) (1.5 MED, p < .004); ubiquinone decreased with 4.2 J/cm(2) (3 MED , p < .0007). A linear decrease in alpha-tocopherol occurred - approxi mately 1.7 pmol tocopherol/cm(2) surface were destroyed per J/cm(2) UV -light. Urate was depleted by irradiation with 8.4 J/cm(2) (6 MED), wh ile ascorbate was depleted by 16.8 J/cm(2) (12 MED). Cellular protein carbonyls and lactic dehydrogenase (LDH) leakage into the medium were only increased at 1 h incubation following exposure to 16.8 J/cm(2) (1 2 MED). At 24 h incubation, PGE(2) was increased in the medium of cell s exposed to UV-irradiation at 0.35 J/cm(2) (0.25 MED) compared with s ham-exposed cells (p < .04); higher UV exposures lead to significant i ncreases in both PGE, (p < .001) and LDH (p (.001) in the medium. In c onclusion, human skin equivalents respond to suberythemal levels of UV -irradiation by increasing production of PGE(2); higher levels of UV-i rradiation (at least 1 MED) were needed to deplete cellular antioxidan ts and induce immediately detectable oxidative damage. (C) 1997 Elsevi er Science Inc.