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铁离子通过羟基和非羟基自由基机制对DNA的光敏损伤。

Ferric-ion-photosensitized damage to DNA by hydroxyl and non-hydroxyl radical mechanisms.

作者信息

Larson R A, Lloyd R E, Marley K A, Tuveson R W

机构信息

Institute for Environmental Studies, University of Illinois, Urbana-Champaign 61801.

出版信息

J Photochem Photobiol B. 1992 Jul 30;14(4):345-57. doi: 10.1016/1011-1344(92)85113-9.

DOI:10.1016/1011-1344(92)85113-9
PMID:1403376
Abstract

Iron(III) and UVA (320-400 nm) light strongly diminished the transforming activity of Haemophilus influenzae DNA in the presence of oxygen. Iron(III) alone in the absence of light had no measurable effect on the transforming activity. The chelating agent ethylenediaminetetraacetic acid (EDTA) conferred virtually complete protection, but hydroxyl radical scavengers (mannitol, methanol, ethanol, isopropanol and dimethyl sulfoxide) inhibited only a small fraction of the inactivation. Treatment of plasmid DNA (pBR322) with iron(III) results in the conversion of the covalently closed circular form of the plasmid to open circles and ultimately to the linear form. Concomitant with the alteration in the conformation of the plasmid, the ability to transform Escherichia coli was reduced. In model systems, iron(III) photoreacted with the DNA backbone causing nicking and double-strand breakage. The results are consistent with a mechanism involving a preliminary complexation of iron(III) by DNA followed by the generation of reactive free radicals other than .OH. We suggest that bound iron, or other UV-absorbing transition metal complexes, may be chromophores capable of causing DNA damage in the long-wave near-UV region.

摘要

在有氧存在的情况下,铁(III)和UVA(320 - 400纳米)光会显著降低流感嗜血杆菌DNA的转化活性。在无光条件下单独的铁(III)对转化活性没有可测量的影响。螯合剂乙二胺四乙酸(EDTA)几乎能提供完全保护,但羟基自由基清除剂(甘露醇、甲醇、乙醇、异丙醇和二甲亚砜)仅能抑制一小部分失活。用铁(III)处理质粒DNA(pBR322)会导致质粒的共价闭合环状形式转变为开环形式,并最终转变为线性形式。伴随着质粒构象的改变,其转化大肠杆菌的能力降低。在模型系统中,铁(III)与DNA主链发生光反应,导致切口和双链断裂。这些结果与一种机制相符,该机制涉及铁(III)首先与DNA形成复合物,随后产生除·OH之外的活性自由基。我们认为结合的铁或其他吸收紫外线的过渡金属络合物可能是能够在长波近紫外线区域引起DNA损伤的发色团。

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