1. IntroductionAttention-deficit hyperactivity disorder (ADHD) is an early-onset, highly prevalent neurobehavioral disorder with genetic,environmental and biologic etiologies, that persists into adoles-cence and adulthood in a sizable majority of afflicted children ofboth sexes. It is characterized by behavioral symptoms ofinattention, hyperactivity, and impulsivity across the life cycle[1,2]. Oxidative stress is an important contributing factor in thepathogenesis of many pediatric diseases, including dyslexia,autism, Down syndrome and ADHD [3,4]. Increased productionof free radicals and also oxidative stress may cause the alterationsinthehomeostasisofsometraceelements[5].Traceelementssuchas Cu, Zn, Fe and Se play a pivotal role in the oxidant/antioxidantmechanism, imbalance of which leads to increased susceptibilityto oxidativedamageof tissuestherebyleadingto thepathogenesisof many diseases. Some studies have confirmed that the metals,including Cu, Fe, Cd, Cr, and Pb participate in the produce of freeradicals resulting in DNA damage, lipid peroxidation, depletion ofglutathione and protein-bound sulphydryl groups and the othereffects [6,7].It has been reported [8,9] that the symptoms of ADHD may becaused by catecholamine dysfunction, particularly imbalances inthe dopaminergic and noradrenergic systems. Copper is necessaryforthecatalyticactivityofenzymeswhichplaysanessentialroleinneurobiology and disease [4,10], including tyrosinase for melaninsynthesis, Cu/Zn superoxide dismutase for antioxidant defense,dopamine b-hydroxylase for catecholamine biosynthesis andceruloplasmin for brain iron homeostasis. The best-knownantioxidative role of Cu is that of being the major cofactor inCu/Zn superoxide dismutase. This enzyme is involved in theprotection of cells from free radicals therefore the depletion ofcopper leads to decreased capability of cells to produce Cu/Znsuperoxide dismutase and thus increasing their propensity tooxidative damage. On the other hand, Cu acts as a pro-oxidant and