Role of Oxygen Intermediates in UV-Induced Epidermal Cell Injury

To investigate the role of oxygen intermediates (OIs) in sunburn cell (SC) formation and development of UV- inflammation in vivo, groups of mice were injected in- travenously 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 SCs per unit length of ear epidermis was counted using hematoxylin- eosin stained sections. The number of SCs was significantly decreased (p < 0.02) by a single injection of SOD (10–30 units/g body weight) 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. These findings suggest that Ols generated by UVR participate in SC formation but are not apparently involved in UV-edema