Evaluation of antioxidant activity of emulsan <i>in vitro</i>

Abstract

Oxidative stress has been involved in the development of several pathologies, including vascular damage associated to myocardial and neurological degeneration, such as arteriosclerosis, cerebral ischemia among others; while diabetes, rheumatoid arthritis, inflammation, cancer-initiation, and acceleration of the aging processes are also reported (Coyle and Puttfarcken, 1993; Margail et al., 2005). The toxicity of oxidative stress is believed to be caused by Reactive Oxygen and Nitrogen Species (ROS and RNS, respectively) that can initiate a wide range of oxidative toxic reactions in biological systems (Cuzzocrea et al., 2001). Typical radicals and radical-related toxic molecules produced by ROS are hydrogen peroxide (H2O2), hydroxyl radical (OH⋅), singlet oxygen (1O2), and superoxide anion radical (O2 ⋅-) (Figure 1). The RNS toxic reactants include nitric oxide (NO⋅) and the most powerful oxidant peroxynitrite anion (ONOO-). Biological antioxidant mechanisms described in the literature are many, but with different efficiencies implicating enzymatic as well as non-enzymatic activities. Some of the most relevant antioxidative biocatalysts are superoxide dismutase, and catalase. In addition, other specialized enzymes such as glutathione peroxidase and ã-glutamylcysteine synthetase can be involved in deactivation mechanisms (Figure 1). Well-known non-enzymatic antioxidants are b-carotene, glutathione, melatonin and vitamins C and E, (Valko et al., 2006). However, excessive and persistent formation of free radicals could be main factors of genotoxic effects.