The Effects of Melon Superoxide Dismutase and Gliadin on Glutathione Reductase (GSH) and Superoxide Dismutase (SOD) Levels in Blood Plasma and Vitreoretina in Diabetic Rat Model: A Literature Review

Abstract

Chronic hyperglycemia in diabetics causes microvascular damage through four mechanisms of biochemical changes, including activated protein kinase C (PKC) pathway, activated hexosamine pathway, increased polyol pathway, and increased advanced glycation end-products (AGEs), all of which will increase Reactive Oxygen Species (ROS) levels. ROS can damage proteins, nucleic acids, and lipids and hasten the onset of diabetes. ROS are produced in the presence of normal blood sugar levels, and the natural breakdown of glucose is controlled by insulin. Variables that regulate cellular respiration, including NAD-related substrates, oxygen, succinate, and antioxidant enzymes, modulate ROS levels and sustain cellular redox equilibrium. The conversion of superoxide anions into hydrogen peroxide, before subsequently metabolized into water by catalase and glutathione (GSH) peroxidase, is facilitated by the metalloprotein superoxide dismutase (SOD). Increased ROS levels can lead to diabetic complications, one of which is diabetic retinopathy. Melon superoxide dismutase (SOD) combined with gliadin (Glisodin®) is a potent antioxidant in counteracting free radicals that can reduce oxidative stress and prevent further cell death. Research related to the use of Glisodin® shows potential as an antioxidant agent with the hope of preventing diabetic complications