金属离子及其络合物在增强生物系统损伤或保护这些系统免受O2−毒性中的作用和机制

Sara Goldstein, Gidon Czapski
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引用次数: 151

摘要

1,10-菲罗啉和一些取代的1,10-菲罗啉的库珀配合物在还原剂和分子氧的存在下切割DNA。一般来说,损伤是由于通过Haber-Weiss反应形成的羟基自由基造成的。假设该反应发生在与生物靶点的三元金属配合物上,其机制定义为“位点特异性机制”。在这些系统中,O2−通过铜(II)的还原来驱动循环。另一方面,这些铜配合物催化O2 -的突变,从而保护系统免受O2 -毒性。本文从动力学角度解释了这些配合物的毒性。对可能导致金属离子或其配合物作为O2−毒性的保护剂或敏化剂的各种因素进行了一般性讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role and mechanism of metal ions and their complexes in enhancing damage in biological systems or in protecting these systems from these systems from the toxicity of O2−

Cooper complexes of 1,10-phenanthroline and some substituted 1,10-phenanthroline cleave DNA in the presence of a reducing agent and molecular oxygen. Generally, the damage is attributed to hydroxyl radicals which are formed through the Haber-Weiss reaction. It is assumed that this reaction occurs with the ternary metal complexes with the biological target and the mechanism is defined as the “site specific mechanism.” In these systems, O2 drives the cycle through the reduction of copper(II). On the other hand, these same copper complexes catalyze the dismutation of O2 and thus should protect the systems from O2 toxicity. In this article, the toxicity of these complexes is explained on kinetic grounds. A general discussion on the various factors which could cause the metal ions or their complexes to act either as protectors from O2 toxicity or as sensitizers of toxic effects of O2 is given.

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