CHAPTER ONE

1.1 INTRODUCTION Heart disease(cardiovascular disease), defined as coronary artery disease, hypertensive heart disease, congestive heart failure, peripheral vascular disease, and atherosclerosis including cerebral artery disease and strokes, is the leading cause of death in the United States and disability in the world today, (Thom, 1989). In the United States, the heart disease death toll is nearly one million each year, and in 2002 the estimated cost of heart disease treatment was $326.6 billion, (Shekelle et al., 2003). To provide early prognosis and better therapies for preventing and curing these diseases, an understanding of the basic pathophysiologic mechanisms of heart disease is essential. Growing evidence indicates that oxdant stress production of reactive oxygen species (ROS) and other free radicals under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD). Free radicals are molecules containing one or more unpaired electrons in atomic or molecular orbital, (Gutteridge et al., 2000). Reactive free radicals play a crucial part in different physiological processes ranging from cell signaling, inflammation and the immune defense, (Elahi et al., 2006). There is increasing evidence that abnormal production of free radicals lead to increased stress on cellular structures and causes changes in molecular pathways that underpins the pathogenesis of several important human diseases, including heart disease, neurological disease and cancer and in the process of physiological ageing, (Pacher 2008; Vassalle et al., 2008). One of the major contributors of oxidative stress is the reactive oxygen species (ROS) family of molecules. These include free radicals such as superoxide anion (O2-), hydroxyl radical (HO-), lipid radicals (ROO-) and nitric oxide (NO). Other reactive oxygen species, hydrogen peroxide (H2O2), peroxynitrite (ONOO-) and hypochlorous acid (HOCl), although are not free radicals but they have oxidizing effects that contribute to oxidative stress. ROS has been implicated in cell damage; necrosis and cell apoptosis due to its direct oxidizing effects on macromolecules such as lipids, proteins and DNA, (Izakovic et al., 2006). Production of one free radical can lead to further formation of radicals via sequential chain reactions, (Cronin et al., 2005). Understanding the contribution of free radical stress in the pathogenesis of disease will allow us to study the development of oxidative stress; a condition that occurs due to an imbalance between cellular production of oxidant molecules and the availability of appropriate antioxidants species that defend against them. In physiological conditions, cells would increase activities of antioxidant enzymes and other antioxidant defenses to counteract occurrence of oxidative stress, (Brunzini et al., 2004). These include radical scavengers such as vitamin E, A, beta carotene and vitamin C, Manganese dependent superoxide dismutase such as manganese superoxide dismutase (Mn-SOD), Copper/Zinc superoxide dismutase (Cu/Zn SOD), glutathione peroxidase, glutathione reductae and catalase (CAT). Decreased risk of cardiovascular death has been associated with higher blood levels of vitamin C and E. In addition, vitamin C, vitamin E, and A have demonstrated antioxidant effects, including beneficial effects on oxidation of low-density lipoprotein. There is evidence that these vitamins affect other risk factors for CVD such as hypertension. Vitamin E may also reduce coronary artery blockage by decreasing blood platelet aggregation. Thus, it was reasonable to expect that supplementation with these antioxidants would decrease the risk of developing CVD. Large numbers of people are taking antioxidants with the expectation that they will prevent disease. As part of a natural defense system, antioxidants can mitigate the activity of free radicals and other oxidative species that have been implicated in the development of heart disease, (Krzanowski, 1991; Duthie et al., 1999). The epidemiologic and observational literature has suggested a beneficial effect of antioxidant-rich foods, as well as specific antioxidants, on the risk of CVD and stroke, (Asplund, 2002; Tribble, 1999).

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