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金属酞菁光敏化导致的DNA链断裂和碱基释放

DNA strand scission and base release photosensitized by metallo-phthalocyanines.

作者信息

Gantchev T G, Gowans B J, Hunting D J, Wagner J R, van Lier J E

机构信息

Department of Nuclear Medicine and Radiobiology, Faculty of Medicine, University of Sherbrooke, Québec, Canada.

出版信息

Int J Radiat Biol. 1994 Dec;66(6):705-16.

PMID:7814970
Abstract

Photoirradiation of aqueous solutions of DNA in the presence of Al- or Zn-tetrasulphonated phthalocyanines (AIPcS4 and ZnPcS4) causes formation of strand breaks and liberation of nucleobases. The effect of added D2O, which enhances singlet oxygen (1O2) lifetime, radical scavengers including alcohols and the spin-trap DMPO, as well as superoxide dismutase, indicates that both singlet oxygen (1O2) and free radicals contribute to the production of strand breaks. However, in the case of base release, only free radicals, such as the hydroxyl radical (.OH), appear to be involved in the degradation process. Detection of the characteristic free-radical oxidation products of deoxyribose provides evidence that .OH are involved in the photosensitized DNA damage. EPR and spin trapping data suggest that superoxide (O2.-) is the most likely precursor of .OH and a Fenton-type mechanism is proposed for their formation.

摘要

在铝或锌的四磺化酞菁(AIPcS4和ZnPcS4)存在的情况下,对DNA水溶液进行光照射会导致链断裂并释放出核碱基。添加重水(D2O)(可延长单线态氧(1O2)寿命)、包括醇类的自由基清除剂和自旋捕捉剂DMPO以及超氧化物歧化酶的影响表明,单线态氧(1O2)和自由基都对链断裂的产生有作用。然而,就碱基释放而言,似乎只有自由基,如羟基自由基(·OH)参与了降解过程。对脱氧核糖特征性自由基氧化产物的检测提供了证据,表明·OH参与了光敏化DNA损伤。电子顺磁共振(EPR)和自旋捕捉数据表明,超氧阴离子(O2·-)最有可能是·OH的前体,并提出了一种芬顿型机制来解释它们的形成。

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