Abstract

Oxidative stress is an imbalance between the amount produced and the removal of oxidants produced. In other words, the increase in reactive oxygen species (ROS) or reactive nitrogen species (RNS) and/or the reduction of the antioxidant/intrinsic/extrinsic is the main cause of this problem [1]. This is one of the most important causes of acute and chronic kidney disease [2]. Increasing the accumulation of free radicals within the kidney resulting from the malfunctioning of the antioxidant defense will ultimately lead to acute renal tubule necrosis, impaired function, and ultimately reduced glomerular filtration (GFR) [3]. The important factors of ROS molecules are hypochlorous acid, superoxide anion, hydrogen peroxide and hydroxyl radical. Because ROS molecules are very active, they quickly destroy molecules such as fats, DNA and proteins [4]. The factors that cause elevation of ROS and its products in the kidney cells are inflammatory cytokines, angiotensin II, mechanical pressure, hyperglycemia, protein kinase C (PKC), free fatty acids, TGF-beta1 and NADPH oxidases enzymes (NOXs). NADPH oxidases (NOXs) are enzymes that produce ROS. The NOX family contains seven subgroups (NOX1- 5 and DUOX 1 and 2) [5].