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大鼠肾脏缺血/再灌注损伤中博来霉素可检测铁的增加。

Increase in bleomycin-detectable iron in ischaemia/reperfusion injury to rat kidneys.

作者信息

Baliga R, Ueda N, Shah S V

机构信息

Department of Pediatrics, Louisiana State University School of Medicine, New Orleans.

出版信息

Biochem J. 1993 May 1;291 ( Pt 3)(Pt 3):901-5. doi: 10.1042/bj2910901.

Abstract

Iron has been shown to be important in ischaemic, immune and toxic forms of tissue injury in various organs. Although it is generally accepted that iron participates in the generation of powerful oxidant species (e.g. hydroxyl radicals) there has not been any direct evidence that iron capable of catalysing free-radical reactions is increased in tissues in these models of injury. In the present study we demonstrate that ischaemia/reperfusion injury to the kidney results in no significant change in total, nonhaem or ferritin iron levels, but there is a marked and specific increase in bleomycin-detectable iron (capable of catalysing free-radical reactions) in the kidney. The increase in bleomycin-detectable iron is observed only after reperfusion but not during the ischaemic period. In a separate study we demonstrate that despite a drastic reduction in the iron content in the kidney, as a result of feeding an iron-deficient diet, there is a similar and a marked increase in the bleomycin-detectable iron in kidneys accompanied by a lack of protection against ischaemia/reperfusion injury.

摘要

铁已被证明在各种器官的缺血性、免疫性和毒性组织损伤中起着重要作用。尽管人们普遍认为铁参与了强氧化剂(如羟基自由基)的生成,但尚无直接证据表明在这些损伤模型中,能够催化自由基反应的铁在组织中有所增加。在本研究中,我们证明肾脏的缺血/再灌注损伤并未导致总铁、非血红素铁或铁蛋白水平发生显著变化,但肾脏中可被博来霉素检测到的铁(能够催化自由基反应)有明显的特异性增加。可被博来霉素检测到的铁的增加仅在再灌注后出现,而在缺血期未出现。在另一项研究中,我们证明,尽管通过喂食缺铁饮食使肾脏中的铁含量大幅降低,但肾脏中可被博来霉素检测到的铁仍有类似的显著增加,同时对缺血/再灌注损伤缺乏保护作用。

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