THE EFFECTS OF UVA-I (340-400 NM), UVA-II (320-340 NM) AND UVA-I-VIVO(II ON THE PHOTOISOMERIZATION OF UROCANIC ACID IN)

Ultraviolet B radiation (280-320 nm) can systemically suppress contact hypersensitivity (CHS), delayed type hypersensitivity (DTH) and tumor rejection responses in mice, Several models have been postulated for the initiation of this UVB-induced immune suppression and, although th e complete mechanism is unclear, our early studies suggested that init iation is via the activation of a photoreceptor in the skin, identifie d as urocanic acid (UCA). Recent preliminary data from our laboratory and others indicated that WA (320-400 nm)-emitting broadband sunlamps can also isomerize UCA but may not lead to immune suppression, in cont rast to UVB-emitting sunlamps, which cause both effects, Although the reason for this inconsistency is unknown, the emission spectra of WA l amps contain differing amounts of UVB, UVA-I (340-400 nm) and WA-TI (3 20-340 mn) from those of WB sources. In this study we determined a det ailed dose-response for the isomerization of UCA in mouse skin using t he UVA-I, WA-II and UVA-I+II wavelength ranges. The dose-response curv es obtained were put on an equal energy basis by quantum correction an d the possibility of wavelength interaction for this effect investigat ed, A simple additive wavelength interaction between WA-I, UVA-II, and UVA-I+II was observed for trans-UCA photoisomerization. This result i ndicates that the failure of UVA-I, UVA-II or UVA-I+II radiation to in duce immune suppression of the CHS response in an animal model is not due to complex wavelength interactions and/or the presence of an in vi vo endogenous photosensitizer of UCA isomerization, Other factors, suc h as downstream blocking by UVA of the cis-UCA generated signal, may b e involved.