||P.8 left column 2nd paragraph: "The link between iron and atherosclerosis may be substantiated by the following mechanism. Iron is released from transferrin, ferritin and senescent erythrocytes. Release of iron from transferrin involves protonation of the carbonate anion, loosening the metal–protein bond (Bacon and Tavill 1984). Uptake of transferrin and release of iron occur in the endosome of all cells, and the daily amount of exchanged iron is about 0.03 g. The endosomal iron is poorly ligated and so capable of catalyzing the formation of ROS, increasing thus the oxidative status which in turn causes oxidation of LDL-C [Low-density lipoprotein cholesterol]. Experiments performed using animal models revealed an increased amount of iron in atherosclerotic lesions. Thus, iron-catalyzed formation of ROS [Reactive Oxygen Species] via Fenton chemistry may play a role in the mechanism of atherosclerosis development (Yuan and Li 2003)."