Kruszewski Marcin
Department of Radiobiology and Health Protection, Institute of Nuclear Chemistry and Technology, Dorodna 16, 03-195 Warsaw, Poland.
Mutat Res. 2003 Oct 29;531(1-2):81-92. doi: 10.1016/j.mrfmmm.2003.08.004.
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.
痕量“游离”铁可通过芬顿/哈伯-维伊斯反应循环催化产生剧毒的羟基自由基。关键因素似乎是细胞内不稳定铁池（LIP）的可用性和丰度，它构成了含铁化合物代谢途径的交叉点，处于细胞对铁的需求、摄取和储存之间的中间位置。为避免有害“游离”铁过量，通过对参与铁稳态的主要蛋白质表达进行转录和转录后控制，将LIP维持在最低充足水平。本文讨论了细胞LIP的假定来源、其稳态及其在细胞对氧化应激反应中的作用。
