18 J Cont Med Sci | Vol. 1, No. 2, Spring 2015: 18–22 Research Objective Clinical evidence suggests oxidative stress and inflammation linked to reactive oxygen species (ROS) over generation may be a key in the pathogenesis of certain disease. Cardiovascular disease is one example of this process. ROS have been proposed to be the mediators of inflammation in experimental cardiovascular pathology. Till now, areas with regard to the effects of ROS in the ischemic heart disease (IHD) are not completely understood. The present study was conducted to investigate the involvement of inflammation as a consequence of oxidative stress in the pathology of IHD. Methods Serum lipid profile, trace element, antioxidant enzyme activities [catalase (CAT), superoxide dismutase (SOD)], hydrogen peroxide (H 2 O 2 ) and the inflammation marker (TNF-α and IL-6) were measured in 50 patients with IHD and 50 healthy subjects as control group. All results were statistically analysed. Results A highly significant decrease was found in the serum level of both zinc (Zn) and copper (Cu) in patients with IHD compared to control (P < 0.05). Serum levels of antioxidants (SOD, CAT) were also significantly decreased in the patient group (P < 0.05) compared to control. However, H 2 O 2 and cytokines (TNF-α and IL-6) levels demonstrated a significant increase in IHD patients (P < 0.01). Conclusion The results of the present study provide evidences that oxidative stress, inflammation and trace element are closely linked and involved in IHD that may have future role in developing new therapeutic strategies. Keywords oxidative stress, inflammation, ischemic heart disease, antioxidants, trace elements  Oxidative stress and inflammation in ischemic heart disease: role of trace elements, oxidants and antioxidants Anwar Jasib Thaaban Almzaiel Introduction Heart disease is one of the major health problems of devel- oping countries of the world. Recent research has shown that free radicals, particularly, reactive oxygen species (ROS) play an important role in the pathogenesis of oxidative myocardial damage with consequential cardiac malfunction. 1 Oxidative stress describes the condition where an excessive production of ROS overwhelms endogenous anti-oxidant defense mecha- nisms. e resultant elevation in ROS levels has a detrimental effect on cellular function, a consequence of ROS-induced damage to lipid membranes, enzymes and nucleic acids. Generation of ROS has been involved in various cardio- vascular disorders, including ischemia/reperfusion (I/R), ath- erosclerosis and cardiotoxicity induced by drugs. 2 ese ROS caused an injury to vascular cells and cardiac myocytes directly, and can initiate a series of local chemical reactions that result in an amplification of the initial ROS-mediated car- diomyocyte dysfunction. 3 Oxidative stress is now thought to play an important role in the pathogenesis of coronary heart disease through oxidation of low-density lipoprotein (LDL)-cholesterol and free radical formation. 4 Oxidised LDL-cholesterol aids the evolution of early arterial wall lesions into atherosclerotic plaques by promoting the formation of foam cells from macrophages as well as the recruitment and retention of monocytes in the arterial wall. 5 ROS may con- tribute to atherogenesis by damaging the arterial endothelium, promoting thrombosis and interfering with the normal vaso- motor regulation. It is assumed that antioxidant enzymes, superoxide dis- mutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) constitute a first line of defense against oxidative stress by removing ROS. 6 SOD, catalyses the dismutation of the superoxide anion (O 2 •- ) into hydrogen peroxide (H 2 O 2 ) within cells and in the extracellular matrix, while CAT and GSH-Px remove H 2 O 2 , and GSH-Px can also convert lipid peroxyl rad- icals to nontoxic alcohols. 6 Low levels of activity of these anti- oxidant enzymes have been shown to associate with increased risk of CHD. 3 Recently, inflammation has been linked, both experimentally and clinically, to cardiovascular disease. 7 During inflammation ROS are generated, which can be due to immune cells, such as [dendritic cells (DCs), lymphocytes, neutrophils and macrophages] or interleukins and other inflammatory cytokines, such as tumor necrosis factor (TNF- α). 8,9 Because metals can cause oxidative modification of LDL-cholesterol and the synthesis of ROS, the effect of several prooxidant metals, including Cu on cardiovascular disease has come under investigation. Recent researches demonstrate the importance of certain elements in the pathogenesis of cardio- vascular disorders. Statistically significant positive correla- tions have been found between trace element concentrations (Cu, Zn, Se) of heart tissue with physiological parameters (CO: cardiac output, EF: ejection fraction) of the heart. It is probable that free oxygen radicals and oxidatively modified particles of LDL participate in the development of atheroscle- rotic lesions and the potential role of natural antioxidants (Vit. C - ascorbic acid; Vit. E - tocopherol) is inhibition of this pro- cess. 10 However, understanding of inflammation and ROS, especially with their pathophysiological role in cardiovascular dysfunction, is still unclear and further investigations will facilitate the development and/or delivery of selective Department of Medical Biochemistry, College of Medicine, University of Al-Qadisiyah, Qadisiyyah, Iraq. Correspondence to Anwar Jasib Thaaban Almzaiel (email: vipvip128@yahoo.com) (Submitted: 13 January 2015 – Revised version received: 10 April 2015 – Accepted: 25 April 2015 – Published online: Spring 2015)