The labile iron pool of cells (LIP) constitutes the primary source of
metabolic and catalytically reactive iron in the cytosol. We studied L
IP homeostasis in K562 cells using the fluorescent metal-sensitive pro
be calcein. Following brief exposure to iron(II) salts or to oxidative
or reductive stress, LIP rose by up to 120% relative to the normal le
vel of 350 nM. However, the rate of recovery to normal LIP level diffe
red markedly with each treatment (respective t(1/2)s of 27, 65-88 and
less than or equal to 17 min). We show that the capacity of K562 cells
to adjust LTP levels is highly dependent on the origin of the LIP inc
rease and on the pre-existing cellular iron status.