Häder Donat-P, Sinha Rajeshwar P
Institut für Botanik und Pharmazeutische Biologie, Friedrich-Alexander-Universität, Staudtstr. 5, D-91058 Erlangen, Germany.
Mutat Res. 2005 Apr 1;571(1-2):221-33. doi: 10.1016/j.mrfmmm.2004.11.017. Epub 2005 Jan 25.
Continuing depletion of stratospheric ozone and subsequent increases in deleterious ultraviolet (UV) radiation at the Earth's surface have fueled the interest in its ecological consequences for aquatic ecosystems. The DNA is certainly one of the key targets for UV-induced damage in a variety of aquatic organisms. UV radiation induces two of the most abundant mutagenic and cytotoxic DNA lesions, cyclobutane pyrimidine dimers (CPDs) and pyrimidine pyrimidone photoproducts (6-4PPs) and their Dewar valence isomers. However, aquatic organisms have developed a number of repair and tolerance mechanisms to counteract the damaging effects of UV on DNA. Photoreactivation with the help of the enzyme photolyase is one of the most important and frequently occurring repair mechanisms in a variety of organisms. Excision repair, which can be distinguished into base excision repair (BER) and nucleotide excision repair (NER), also play an important role in DNA repair in several organisms with the help of a number of glycosylases and polymerases, respectively. In addition, mechanisms such as mutagenic repair or dimer bypass, recombinational repair, cell-cycle checkpoints, apoptosis and certain alternative repair pathways are also operative in various organisms. This review deals with the UV-induced DNA damage and repair in a number of aquatic organisms as well as methods of detecting DNA damage.
平流层臭氧的持续消耗以及随后地球表面有害紫外线（UV）辐射的增加，引发了人们对其对水生生态系统生态后果的关注。DNA无疑是多种水生生物中紫外线诱导损伤的关键靶点之一。紫外线辐射会诱导两种最常见的诱变和细胞毒性DNA损伤，即环丁烷嘧啶二聚体（CPD）和嘧啶嘧啶酮光产物（6-4PPs）及其杜瓦价键异构体。然而，水生生物已经发展出多种修复和耐受机制来抵消紫外线对DNA的破坏作用。在光解酶的帮助下进行光复活是多种生物中最重要且最常发生的修复机制之一。切除修复可分为碱基切除修复（BER）和核苷酸切除修复（NER），在多种生物的DNA修复中，分别借助多种糖基化酶和聚合酶也发挥着重要作用。此外，诸如诱变修复或二聚体旁路、重组修复、细胞周期检查点、细胞凋亡以及某些替代修复途径等机制在各种生物中也发挥作用。本综述探讨了多种水生生物中紫外线诱导的DNA损伤与修复以及检测DNA损伤的方法。
