Diabetes mellitus (DM) is an endocrine disorder characterized by impaired insulin secretion or peripheral tissue resistance to the effects of insulin (Wild et al.,2004; Ali et al., 2014; Shah and Khan, 2014). The complex etiology of DM has previously been discussed 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 shown a link between Type 1 DM and decreased ROS antagonist and scavenging enzyme activity, which results in metabolic disturbances (Evans et al., 2002; Kumaret al., 2013) and oxidative stress-induced tissue damage (Kesavulu et al., 2000; Yue et al., 2003; Shah and Khan, 2014). (Ahmed et al., 2010; Ali et al., 2014) and side effects like nephropathy, neuropathy, microangiopathy, ketoacidosis, retinopathy, and neuropathy (Rameshkumar et al., 2004; Pop-Busui et al., 2006; Yim et al., 2007; Singh et al., 2011). Stress-sensitive signaling pathways, which are the origins of DM pathology and complications, are linked to molecular events that cause -cell dysfunction and insulin resistance (Evans et al., 2002; Malviya et al., 2010; Aliet al., 2014). In order to induce Type 1 DM in laboratory animals, alloxan or streptozotocin salt solutions are frequently injected intraperitoneally. This is because these drugs specifically damage pancreatic -cells through oxidative stress (Takasu et al.,2001; Szkudelski, 2001; Yim et al., 2007; Shah and Khan, 2014). The current theory regarding the mechanism underlying diabetes and diabetic complications points to oxidative stress (Halliwell and Gutteridge, 1989). The body continuously produces free radicals. as a result of interactions between regular metabolic processes and environmental stimuli. Numerous antioxidant defenses guard against the harmful effects of free radical production in vivo under physiological conditions (Halliwell and Gutteridge, 1989). Oxidative stress is caused by an imbalance between the systems that produce and remove free radicals, which can occur when the production of free radicals increases or the activity of antioxidant defenses decreases, or when both of these phenomena occur. Free radicals may be produced in diabetes by protein glycation and glucose autoxidation, which then catalyze lipid peroxidation (Mullarkey et al., 1990; baynes, 1991). Ascorbic acid levels decreased, glutathione metabolism was impaired, and antioxidant defense systems were disturbed in diabetics, according to Strains (1991), McLennan et al. (1991), and other studies (Jennings et al.,1987; Young et al., 1992).


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