Normal cellular metabolism involves the production of ROS, and in humans, superoxide (O2 -) is the most commonly produced free radical. Phagocytic cells such as macrophages and neutrophils are prominent sources of O2 -. During an inflammatory response, these cells generate free radicals that attack invading pathogens such as bacteria and, because of this, the production of O2- by activated phagocytic cells in response to inflammation is one of the most studied free radical producing systems. The majority of the H2O2 is broken down to O2 and water by the antioxidant enzyme catalase. In addition to catalase, glutathione peroxidase can also break down H2O2 and also any peroxides that form on lipids within the body [5]. When O2 - reacts with nitric oxide (NO), the toxic product peroxynitrite (ONOO-) is formed. Cellular ROS originate from O2- generated as a by-product of oxidative phosphorylation (mitochondrial respiration), they differ in their mechanism of production, necessary cofactors, diffusion range, hydrophobicity, biological targets, detoxification pathways and breakdown products. O-2 damaging reactions largely involve disassembly of iron-sulphur clusters in proteins. H2O2 or O-2 alone lacked reactivity toward iron regulatory protein-1 (IRP-1), but a combined action of the two species induced reversible inactivation of IRP-1. Such an effect was attributed to direct interactions of O-2 and H2O2 with a preformed pool of IRP-1, resulting in reversible modifications of -SH residues; in fact, its action would be limited to removing only iron atoms, an effect sufficient to abolish enzyme activity. The hydroxyl radical (.OH) is the most reactive of the free radical molecules. OH- damages cell membranes and lipoproteins by a process termed lipid peroxidation. In fact, lipid peroxidation can be defined as the process whereby free radicals 'steal' electrons from the lipids in our cell membranes, resulting in cell damage and increased production of ROS. This process takes place in 3 stages:

- 1. Initiation: In a peroxide-free lipid system, the initiation of a peroxidation sequence refers to the attack of an ROS (with sufficient reactivity) able to abstract a hydrogen (H) atom from a methylene group (- CH2-).
- 2. 2. Propagation: A peroxyl radical is able to abstract H from another lipid molecule (adjacent fatty acid), especially in the presence of metals such as copper or iron, thus causing an autocatalytic chain reaction. The peroxyl radical combines with H to give a lipid hydroperoxide (or peroxide).
- 3. Termination: formation of a hydroperoxide. Lipid peroxidative damage to lipids in low-density lipoprotein (LDL) plays an important role in atherosclerosis [9]. To protect against oxidative damage, organisms have developed a variety of antioxidant defenses that include proteins, compounds such as vitamins, and specialized antioxidant enzymes.

Lipid-soluble antioxidants are located in the cellular membranes and lipoproteins, whereas the water- soluble antioxidants are present in the aqueous environments, such as fluids inside cells and in the blood. Preventative antioxidant enzymes inside the cell are an important defense against free radicals. In humans, the highest levels of SOD are found in the liver, adrenal gland, kidney, and spleen [10]. Catalase and glutathione peroxidase both work to detoxify O2-reactive radicals by catalyzing the formation of H2O2 derived from O2 -. The liver, kidney, and red blood cells possess high levels of catalase, which helps to detoxify chemicals in the body. The water-soluble tripeptide-thiol glutathione