氮丙啶基硝基咪唑RSU 1069对双链DNA的失活与修复
Inactivation and repair of double-stranded DNA damaged by the aziridinyl nitroimidazole RSU 1069.
作者信息
Lafleur M V, Westmijze E J, Visser O J, Wagenaar N, Soetekouw R, Loman H, Retel J
机构信息
Department of Biophysics, Vrije Universiteit, Amsterdam, The Netherlands.
出版信息
Chem Biol Interact. 1992 Mar;82(1):55-71. doi: 10.1016/0009-2797(92)90014-c.
Incubation of RSU 1069 in the presence of biologically active double-stranded phi X174 DNA resulted in, depending on pH, ionic strength and concentration of drug, inactivation of the DNA. A variety of lesions are induced including a high number of single-strand breaks and alkali-labile lesions, which are at most partly lethal. The main inactivating damage consists probably of base damage, induced by alkylation. A considerable part of the damage induced by RSU 1069 can be repaired by the various repair enzymes of the bacterial host of the phi X174 DNA. Finally the damage (pattern) depends considerably on the ionic composition of the reaction solution, which can be explained by an equilibrium model presented in this paper.
在具有生物活性的双链φX174 DNA存在的情况下孵育RSU 1069，根据pH值、离子强度和药物浓度的不同，会导致DNA失活。会诱导产生多种损伤，包括大量单链断裂和碱不稳定损伤，这些损伤至多部分具有致死性。主要的失活损伤可能由烷基化诱导的碱基损伤组成。RSU 1069诱导的相当一部分损伤可被φX174 DNA细菌宿主的各种修复酶修复。最后，损伤（模式）在很大程度上取决于反应溶液的离子组成，本文提出的平衡模型可以对此进行解释。
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