Terrian D L, Kuhl C N, Tessman I, Morrison H
Department of Chemistry, Purdue University, West Lafayette, IN 47907-1393, USA.
Photochem Photobiol. 1996 Jun;63(6):898-900. doi: 10.1111/j.1751-1097.1996.tb09648.x.
It has been reported that UV-induced immunosuppression can be reversed by photoreactivation or exposure to T4 endonuclease V, two treatments that can repair cyclobutane pyrimidine dimers. These observations, together with the known role of urocanic acid (UA) in UV-induced immune suppression, prompted us to study the ability of DNA photolyase to repair UA-DNA cyclobutane photoadducts in single-stranded calf thymus DNA. We did not detect any release of UA, with a sensitivity implying that photolyase is at least 2900 times less active toward UA-DNA adducts than toward cis-syn thymine-thymine dimers. This indicates that any reversal of photoimmunosuppression by photoreactivation cannot significantly involve cleavage of UA-DNA cyclobutane adducts.
据报道,紫外线诱导的免疫抑制可通过光复活或暴露于T4内切核酸酶V来逆转,这两种处理方法均可修复环丁烷嘧啶二聚体。这些观察结果,连同尿刊酸(UA)在紫外线诱导的免疫抑制中的已知作用,促使我们研究DNA光解酶修复单链小牛胸腺DNA中UA-DNA环丁烷光加合物的能力。我们未检测到UA的任何释放,其灵敏度表明光解酶对UA-DNA加合物的活性比对顺式-胸腺嘧啶-胸腺嘧啶二聚体的活性至少低2900倍。这表明光复活对光免疫抑制的任何逆转都不太可能显著涉及UA-DNA环丁烷加合物的裂解。