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Received Apr 13, 2017; Accepted Jul 3, 2017
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1. Introduction
Ferric nitrilotriacetate (Fe-NTA), a complexation of nitriloacetic acid with iron, has been described as a highly reactive compound and used in several studies to induce hyperglycemia, glycosuria, and both renal and liver carcinogenesis [1, 2]. Previous studies have demonstrated that the major pathway of Fe-NTA toxicity is through the generation of free radicals such as reactive oxygen species (ROS) [1, 3]. ROS cause alterations in the hepatic glutathione metabolizing enzyme, peroxidation of lipids, deterioration of proteins, and ultimately cellular and tissues injuries [1]. Previous research has demonstrated that a vast range of neurodegenerative diseases and the brain aging are correlated with oxidative stress [4–7]. The metabolism of the excitatory amino acid contributes significantly to the generation of ROS in the brain where they are particularly active. The presence of postmitotic cells such as glial cells which have a high predisposition to oxidative alteration amplifies the deleterious effects of ROS in the brain and may lead to the development of brain tumor, stroke, and other disorders [4]. Therefore, Fe-NTA produces an alteration of enzymatic processes and necrosis of hepatocytes in the liver whereas it causes an acute and subacute necrosis of the proximal tubule and renal DNA damage [1]. Fe-NTA has been used previously to induce a variety of disorders to investigate the biological properties of natural compounds against cancer, diabetes, and oxidative mediated toxicity in experimental settling both in vitro and in vitro [1, 3]. Recently, the mechanism of Fe-NTA induced toxicity has been described through its ability to cause an increase in lipid peroxidation and decrease in the concentration of enzymatic and nonenzymatic antioxidant molecules [1]. Epidemiological and biological data have both reported the beneficial impact of diet in the management...