Recent reports have detected the presence of iron in human atheroscler
otic lesions [Biochem. J. 286 (1992) 901-905]. This study provides evi
dence for a biochemical mechanism whereby iron is released from myoglo
bin by low density lipoprotein (LDL) which has become oxidised by the
ferryl myoglobin species. The haem destabilisation and iron release ar
e inhibited by monohydroxamate compounds and desferrioxamine through t
heir ability to inhibit the propagation of LDL oxidation. Thus, iron m
ay derive from the myoglobin released from ruptured cells in the oxidi
sing environment of the atherosclerotic lesion.