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

Abstract

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.