INTRODUCTION
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; Kumar et 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 β–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; Ali et al., 2014). Since alloxan or streptozotocin causes selective oxidative damage to pancreatic β–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 a 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).
The kidneys regulate blood ions and pH levels as well as water balance. In addition, the kidneys serve as principal organ for the elimination of metabolic waste products. The functional unit of the kidney is the nephron and each kidney contains approximately two million of these structures.
Sodium glutamate or monosodium glutamate (MSG) is a major dietary component, which intensifies the savory flavor in foods worldwide (Eweka and Iniabohs, 2007; George et al., 2013; Nwajei et al., 2015). It has a daily consumption rate of 300–4000 mg/day in developed countries (Sharma et al., 2013; Husarova and Ostatnikova, 2013). The toxicity concerns and secondary physiologic effects following intake of MSG have been controversially discussed (Maluly, 2013; Boonnate et al., 2015). LD50 of sodium glutamate in rats ranges between 15000 and 18000 mg/kg of body weight (Walker and Lupien, 2000; Kolawole, 2013).
Meanwhile, certain chemical agents and dietary components perturb blood physiologic homeostatic parameters, such as distortion of plasma testosterone/estrogens concentrations with attendant hormonal imbalance and reproductive disorders, alterations in blood lipid profile associated with the development of atherogenicity as well as provoking the overwhelming level of oxidative stress (Ojo et al., 2006; Svalheim et al., 2008; Bitter et al., 2009; Ibegbulem and Chikezie, 2012; Deavall et al., 2012; Asare et al., 2014). Furthermore, dietary component may alter the weights of visceral organs, which is diagnostic for the atrophic or hypertrophic dysfunctional organs (Amresh et al., 2008).
Accordingly, the present study was carried out to investigate the functional status of renal tissues of alloxan-induced diabetes mellitus rats treated with monosodium glutamate/ascorbic acid.