Diabetes mellitus (DM) is an endocrine disorder associated with poor secretion of insulin or resistance to insulin actions by peripheral tissues (Wild et al.,2004; Ali et al., 2014; Shah and Khan, 2014). The multifaceted etiology of DM has been described elsewhere (El-Missiry and El-Gindy, 2000; Nagappa et al.,2003; Jung et al., 2006; Filippi and von Herrath, 2008; Gwarzo et al., 2010; Trna et al., 2012). Studies have established a connection between Type 1 DM and compromised activities of reactive oxygen species (ROS) antagonists and scavenging enzymes (Kesavulu et al., 2000; Yue et al., 2003; Shah and Khan, 2014), which engender disturbances in metabolism (Evans et al., 2002; Kumaret al., 2013) with attendant oxidative stress induced tissue damage (Ahmed et al., 2010; Ali et al., 2014) and complications such as retinopathy, microangiopathy, ketoacidosis, neuropathy and nephropathy (Rameshkumar et al., 2004; Pop-Busui et al., 2006; Yim et al., 2007; Singh et al., 2011).
Molecular events leading to ß–cell dysfunction and insulin resistance are connected with stress-sensitive signaling pathways, which are progenitors of DM pathology and complications (Evans et al., 2002; Malviya et al., 2010; Aliet al., 2014). Since alloxan or streptozotocin causes selective oxidative damage to pancreatic ß–cells, intra-peritoneal injection of their salt solutions is commonly used to induce Type 1 DM in experimental animals (Takasu et al.,2001; Szkudelski, 2001; Yim et al., 2007; Shah and Khan, 2014). Oxidative stress is currently suggested as mechanism underlying diabetes and diabetic complications (Halliwell and Gutteridge, 1989).
Free radicals are continually produced in the body as the result of normal metabolic processes and interaction with environmental stimuli. Under physiological conditions, a wide range of antioxidant defenses protects against the adverse effects of free radical production in vivo (Halliwell and Gutteridge, 1989). Oxidative stress results from an imbalance between radical-generating and radical scavenging systems, that is, increased free radical production or reduced activity of antioxidant defenses or both these phenomena. In diabetes, protein glycation and glucose autoxidation may generate free radicals, which in turn catalyze lipid peroxidation (Mullarkey et al., 1990; baynes, 1991). Moreover, disturbances of antioxidant defense systems in diabetes were shown: alteration in antioxidant enzymes (Strains, 1991), impaired glutathione metabolism (McLennan et al., 1991), and decreased ascorbic acid levels (Jennings et al.,1987; Young et al., 1992).
