Labile iron pool: the main determinant of cellular response to oxidative stress

被引：421

作者：

Kruszewski, M

机构：

[1] Inst Nucl Chem & Technol, Dept Radiobiol & Hlth Protect, PL-03195 Warsaw, Poland

[2] Maria Sklodowska Curie Mem Canc Ctr, Inst Oncol, Dept Expt Hematol, PL-02781 Warsaw, Poland

[3] Maria Sklodowska Curie Mem Canc Ctr, Inst Oncol, Cord Blood Bank, PL-02781 Warsaw, Poland

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2003年 / 531卷 / 1-2期

关键词：

oxidative cellular damage; hydrogen peroxide; iron homeostasis;

D O I：

10.1016/j.mrfmmm.2003.08.004

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

The trace amounts of "free" iron can catalyse production of a highly toxic hydroxyl radical via Fenton/Haber-Weiss reaction cycle. The critical factor appears to be the availability and abundance of cellular labile iron pool (LIP) that constitutes a crossroad of metabolic pathways of iron-containing compounds and is midway between the cellular need of iron, its uptake and storage. To avoid an excess of harmful "free" iron, the LIP is kept at the lowest sufficient level by transcriptional and posttranscriptional control of the expression of principal proteins involved in iron homeostasis. The putative sources of cellular LIP, its homeostasis and its role in the cellular response to oxidative stress are discussed. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：81 / 92

页数：12

共 94 条

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