FUNCTIONAL STATUS OF RENAL TISSUES OF ALLOXAN-INDUCED DIABETES MELLITUS RATS TREATED WITH MONOSODIUM GLUTAMATE/ASCORBIC ACID (200MG/4000MG)
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FUNCTIONAL STATUS OF RENAL TISSUES OF ALLOXAN-INDUCED
DIABETES MELLITUS RATS TREATED WITH MONOSODIUM GLUTAMATE/ASCORBIC ACID
(200MG/4000MG)
ABSTRACT
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 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; Aliet 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 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).
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