The Effects of UVA‐I (340‐400 nm), UVA‐II (320‐340 nm) and UVA‐I+II on the Photoisomerization of Urocanic Acid in vivo

Abstract— 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 the complete mechanism is unclear, our early studies suggested that initiation is via the activation of a photoreceptor in the skin, identified as urocanic acid (UCA). Recent preliminary data from our laboratory and others indicated that UVA (320‐400 nm)‐emitting broadband sunlamps can also isomerize UCA but may not lead to immune suppression, in contrast to UVB‐emitting sunlamps, which cause both effects. Although the reason for this inconsistency is unknown, the emission spectra of UVA lamps contain differing amounts of UVB, UVA‐I (340‐400 nm) and UVA‐II (320‐340 nm) from those of UVB sources. In this study we determined a detailed dose‐response for the isomerization of UCA in mouse skin using the UVA‐I, UVA‐II and UVA‐I+II wavelength ranges. The dose‐response curves obtained were put on an equal energy basis by quantum correction and the possibility of wavelength interaction for this effect investigated. A simple additive wavelength interaction between UVA‐I, UVA‐II, and UVA‐I+II was observed for trans‐UCA photoisomerization. This result indicates that the failure of UVA‐I, UVA‐II or UVA‐I+II radiation to induce immune suppression of the CHS response in an animal model is not due to complex wavelength interactions and/or the presence of an in vivo endogenous photosensitizer of UCA isomerization. Other factors, such as downstream blocking by UVA of the cis‐UCA generated signal, may be involved.