Abstract

Experiments were conducted to determine whether ultraviolet (UV) radiation exerts its effect through the generation of oxygen intermediates on Langerhans cells (LC). Guinea pigs were exposed to one single dose of UVB (0.9-2.7J/cm2), and biopsy specimens were taken 5 days after the irradiation. The population of LC was evaluated using ATPase-stained epidermal sheets. These exposures reduced the number of LC to 20-25% of the original density. On the other hand, superoxide dismutase (SOD) (0.02-0.2 mg), a scavenger of superoxide anion, which had been injected intradermally just before UV radiation, significantly prevented the depletion of LC, although not completely (37-40% of the original density). The injection immediately after the exposure was still significantly effective, but less so. Other scavengers of oxygen intermediates including catalase, D-mannitol, and L-histidine revealed no detectable effect. A single exposure of UVB at doses of 0.3-0.6 J/cm2 did not deplete the ATPase-positive LC. However, the same dose of UVB reduced the number of LC to 70%, when exposed after the injection of an SOD inactivator, diethyldithiocarbamate, possibly due to inactivation of physiologically existing SOD. These observations indicate that oxygen intermediates such as superoxide anion or its subsequent species are generated by UV radiation exposure and damage the epidermal LC.

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