Effects of UVB irradiation on epidermal adenylate cyclase responses in vitro: its relation to sunburn cell formation
✍ Scribed by H. Iizuka; A. Ishida-Yamamoto; S. Kajita; M. Tsutsui; N. Ohkuma
- Publisher
- Springer-Verlag
- Year
- 1988
- Tongue
- English
- Weight
- 500 KB
- Volume
- 280
- Category
- Article
- ISSN
- 0340-3696
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✦ Synopsis
UVB irradiation augmented the betaadrenergic adenylate cyclase response of pig skin epidermis in vitro. The effect was observed 2-4 h following the irradiation and lasted at least for 48 h. There was no significant difference in cyclic AMP phosphodiesterase activity between control and UVB-irradiated epidermis at lower irradiation dose (150 mJ/cm2), which is the dose of the most marked beta-adrenergic augmentation effect. The augmentation effect was specific to the betaadrenergic system; adenosine and histamine adenylate cyclase responses were unchanged or decreased depending on the irradiation dose. Histologically, marked sunburn-cell formation was observed following the UVB irradiation.
It has been suggested that oxygen intermediates generated by ultraviolet radiation participate in sunburncell formation. The addition of superoxide dismutase (SOD) in the incubation medium significantly inhibited sunburn-cell formation. On the other hand, the betaadrenergic augmentation effect was not affected by the addition of SOD. Other scavengers of oxygen intermediates (catalase, catalase + SOD, xanthine, or mannitol) did not inhibit the UVB-induced beta-adrenergic augmentation effect. Further, superoxide-anion generating systems (hypoxanthine-xanthine oxidase system and acetaldehyde-xanthine oxidase system) revealed no stimulatory effect on the beta-adrenergic response of epidermis.
These results indicate that (a) the UVB-induced beta-adrenergic augmentation effect is inherent to skin and does not depend on systemic factors such as inflammatory infiltrates following UVB irradiation; (b) in contrast to sunburn-cell formation, induction of the betaadrenergic adenylate cyclase response is not directly Offprint requests to.