International Journal of Medical and Biomedical Sciences https://www.watchpub/ijmbs/index.htm FERRITIN AND CARDIOVASCULAR RISK IN OBESE PERSONS Dragana Tomic-Naglic 1 , Djordje S. Popovic 1 *, Milena Mitrovic 1 , Jovanka Novakovic-Paro 1 , Biljana Srdic-Galic 2 , Maja Ruzic 3 , Tijana Icin 1 , Ivana Bajkin 1 , Bojan Vukovic 4 , Edita Stokic 1 . 1 Clinic for Endocrinology, Diabetes and Metabolic Disorders, Clinical Center of Vojvodina, Medical Faculty, University of Novi Sad, Serbia 2 Department of Anatomy, Medical Faculty, University of Novi Sad, Serbia 3 Clinic for Infectious Diseases, Clinical Center of Vojvodina, Medical Faculty, University of Novi Sad, Serbia 4 Emergency Center, Clinical Center of Vojvodina, Medical Faculty, University of Novi Sad, Serbia. Article Info: Author(s): Dragana Tomic-Naglic, Djordje S. Popovic*, Milena Mitrovic, Jovanka Novakovic-Paro, Biljana Srdic-Galic, Maja Ruzic, Tijana Icin, Ivana Bajkin, Bojan Vukovic, Edita Stokic. History: Received: 08-02- 2015 Accepted Date: 23-02-2015 Vol 3 (2), pp, 12-17 February ,2015 Corresponding Author: Oboma Y.I. Clinical Center of Vojvodina, Hajduk Veljkova 1, 21000 Novi Sad, Serbia. E-mail: pitstop021@gmail.com Article Type: Full Length Research ISSN: 2315-9954 Abstract A key step for developing atherosclerosis and cardiovascular ischemic diseases is lipid peroxidation. Metabolism of iron is closely associated with oxidative stress and could be contributing cardiometabolic risk factor. Redox-active iron is effectively controlled by ferritin induced sequestration and ferroxidase activity. One source of redox-active iron could be ferritin. Iron-derived reactive oxygen species are involved in pathogenesis of vascular damages, mediating cytotoxicity and inflammation. Inflammatory cytokines increase gene expression to ferritin, and ferritin expression is also increased in atherosclerotic plaque. The objective of the study is the investigation of correlation between ferritin and cardiovascular risk in obese subjects. Subjects and methods: The investigation included 47 obese persons, analyzing body mass index and body composition, fasting blood glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides and ferritin. Familiar affinity for cardiovascular diseases was determined through investigation of presence of cardiovascular diseases in close relatives (parents and siblings) before 65 years of age. Cardiometabolic risk was determined on the basis of Euro 03 Score tables. Results: Ferritin had no influence upon the risk of development of ten years risk for fatal cardiovascular disease. Ferritin indirectly correlated with HDL-cholesterol (p=0.049), and was directly related with familiar affinity for cardiovascular diseases (p=0.028). Subjects with increased total cardiovascular risk (Euro03 Score >5%) had higher mean ferritin value than those with lower risk score (Euro03 Score <5%). Conclusions: Ferritin represents dependent but important predictor of cardiovascular risk if it is analyzed together with the decreased values of HDL-cholesterol and familiar affinity for ischemic heart disease. Keywords: obesity, ferritin, iron, cardiovascular risk. INTRODUCTION A key step for developing atherosclerosis and cardiovascular ischemic diseases is lipid peroxidation and generation of oxidized low density lipoprotein (LDL) particles. Oxidized LDL is up taken by scavenger- receptor leading to foam cell formation and starting inflammation in artery wall, accelerating process of atherosclerosis (Baker et al., 2008). Vascular smooth muscle cells (VSMC) are stimulated with inflammatory cytokines, inhibiting NO production significantly and increasing cardiovascular risk. Also, release of vascular endothelial growth factor is reduced by cytokines, developing revascularization disability in hypoxemic region and state of oxidative stress (Dulak et al., 2004). It is well known that the metabolism of iron is closely associated with oxidative stress and could be cardiometabolic risk factor. Redox-active iron is effectively controlled by ferritin induced sequestration and ferroxidase activity. One source of redox-active iron could be ferritin. Iron-derived reactive oxygen species are involved in pathogenesis of vascular damages, mediating cytotoxicity and inflammation (Balla et al., 2007). It is very important to mention that inflammatory cytokines increase the expression of ferritin and that ferritin expression is also increased in atherosclerotic plaque (Fernandez-Real et al., a, 2002). Moreover, free radical production and oxidative stress lead to thrombosis and interfere with typical vasomotor regulation (Balla et al., 2007). The fraction of unused and highly toxic iron in an organism is neutralized and put down by binding with apoferritin protein, which result is a complex ferritin molecule. The heavy chain of apoferritin stimulates ferroxidase activity that catalyses the oxidation Fe 2+ into Fe 3+ , which prevents iron-induced cyclic redox reaction that could possibly lead to cell