STUDY OF SERUM IRON AND FERRITIN IN PATIENTS WITH ISCHEMIC HEART DISEASES

Abstract

The oxidative modification of low density lipoprotein, as well as, its uptake by macrophages in vessel wall via scavenger receptors are considered important steps in the development of the atheromatous lesion. This uptake is not down regulated by the intemalized cholesterol and cholesteryl esters and lead to their transformation to cells with the characteristic properties of lipid laden foam cells. It has been shown that low density lipoprotein modification is due to free radical reaction and both copper and iron in reduced fonns are able to induce such process. To promote free radical production, iron must be liberated from proteins. It is believed that oxidant stress itself can provide the iron necessary for formation of reactive oxygen species, for example, by mobilizing iron from ferritin or by degrading heme proteins to release 1ron. Theoretically, ferritin as an iron binding protein may be considered as one of the primary antioxidants that inhibits lipid peroxidation but many evidences contrast this hypothesis. A reductive mechanism is probably responsible for the release of iron from ferritin into the low. molecular weight pool, where it could induce lipid peroxidation and subsequent tissue injury by Fenton type reaction.