Mullokandov E A, Franklin W A, Brownlee M
Department of Radiation Oncology, Albert Einstein College of Medicine, Bronx, NY 10461.
Diabetologia. 1994 Feb;37(2):145-9. doi: 10.1007/s001250050085.
In order to evaluate whether base modifications, apurinic/apyrimidinic site formation, strand breaks, or a combination of these lesions results from the interaction of glycation products with DNA, plasmid DNA was first reacted with these products, and then subjected to digestion with endonuclease III and endonuclease IV of Escherichia coli. Analysis of the differential effects of digestions with these enzymes by electrophoresis on agarose gels demonstrated that reactive glycation products produce both base modification and apurinic/apyrimidinic sites in DNA, in addition to the strand breaks observed after incubation with glycation products alone. These types of DNA damage may occur in specific diabetic cells where elevated levels of glycating sugars are associated with pathologic dysfunction.
为了评估碱基修饰、脱嘌呤/脱嘧啶位点的形成、链断裂，或者这些损伤的组合是否是由糖化产物与DNA相互作用导致的，首先将质粒DNA与这些产物反应，然后用大肠杆菌的核酸内切酶III和核酸内切酶IV进行消化。通过琼脂糖凝胶电泳分析这些酶消化的差异效应表明，活性糖化产物除了在单独与糖化产物孵育后观察到的链断裂外，还会在DNA中产生碱基修饰和脱嘌呤/脱嘧啶位点。这些类型的DNA损伤可能发生在特定的糖尿病细胞中，在这些细胞中，糖化糖水平升高与病理功能障碍相关。
