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.
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.
复制标题
UVA-I (340-400 nm)、UVA-II (320-340 nm) 和 UVA-I II 对体内尿刊酸光异构化的影响。
DOI：
10.1111/j.1751-1097.1997.tb03177.x
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发表时间：
1997
影响因子：
3.3
通讯作者：
DeFabo,EC
中科院分区：
文献类型：
--
作者：
Webber,LJ;Whang,E;DeFabo,EC
紫外线B辐射（280 - 320 nm）可全身抑制小鼠的接触性超敏反应（CHS）、迟发型超敏反应（DTH）和肿瘤排斥反应。对于这种UVB诱导的免疫抑制的启动已经假设了几种模型，尽管完整的机制尚不清楚，但我们早期的研究表明，启动是皮肤中感光细胞的病毒激活，被鉴定为尿刊酸（UCA）。我们实验室和其他人最近的初步数据表明，UVA（320 - 400 nm）发射的宽带日光灯也可以异构化UCA，但可能不会导致免疫抑制，而UVB发射的日光灯会导致这两种效果。虽然这种不一致的原因尚不清楚，但UVA灯的发射光谱包含与UVB源不同数量的UVB、UVA-I（340 - 400 nm）和UVA-II（320 - 340 nm）。在本研究中，我们使用UVA ‐ I、UVA ‐ II和UVA ‐ I + II波长范围测定了小鼠皮肤中UCA异构化的详细剂量反应。通过量子校正将获得的剂量响应曲线置于等能量基础上，并研究了这种效应的波长相互作用的可能性。对于trans-UCA光异构化，观察到UVA-I、UVA-II和UVA-I + II之间的简单加和波长相互作用。该结果表明，UVA-I、UVA-II或UVA-I + II辐射未能诱导动物模型中CHS反应的免疫抑制并非由于复杂的波长相互作用和/或UCA异构化的体内内源性光敏剂的存在。其他因素可能也参与其中，例如UVA对cis-UCA产生的信号的下游阻断。
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 isviathe 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 fortrans‐UCAphotoisomerization. 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 anin vivoendogenous photosensitizer of UCA isomerization. Other factors, such as downstream blocking by UVA of thecis‐UCA generated signal, may be involved.