ROLE OF OXYGEN INTERMEDIATES IN UV-INDUCED EPIDERMAL-CELL INJURY

To investigate the role of oxygen intermediates (OI) in sunburn cell (SC) formation and development of UV-inflammation in vivo, groups of mice were injected i.v. with OI scavengers, including bovine blood superoxide dismutase (SOD), bovine liver catalase, L-histidine, D-mannitol and saline (controls) before and/or after UV irradiation with sunlamp tubes (mainly 280-320 nm; 300 mJ/cm2; UVR). Ear thickness was measured before and 6 and 24 h after UVR. Ears were removed 24 h after UVR and the number of SC per unit length of ear epidermis was counted using hematoxylineosin stained sections. The number of SC was significantly decreased (P < 0.02) by a single injection of SOD (10-30 units/g body wt) given either just before or immediately after (< 15 min) UVR, while SC formation was no longer suppressed by injections given more than 2 h before or after UVR. Four repeated injections of SOD (10 units/g) also reduced SC counts but did not significantly alter ear-swelling responses (ESR). Neither SC counts nor ESR were remarkably suppressed by 4 injections of any of the other active OI scavengers, inactivated SOD, or bovine serum albumin. A single injection of diethyldithiocarbamate, an SOD inactivator, significantly augmented SC formation (P < 0.05), but did not change ESR. OI generated by UVR participate in SC formation but are not apparently involved in UV-edema.