Metabolite of tryptophan promoting changes in EEG signal and the oxidative status of the brain Rosana Ferrari 1,2 *, Silvana Maria Picolli Pugini 2 , Aldo Ivan Cespedes Arce 2 , Ernane Jose Xavier Costa 2 and Mariza Pires de Melo 2 1 Department of Biological Science, State University of Santa Cruz (UESC), Ilhéus, Bahia, Brazil 2 Laboratory of Biological Chemistry, Department of Basic Sciences, Faculty of Animal Science and Food Engineering (FZEA), University of São Paulo (USP), Pirassununga, São Paulo, Brazil Tryptophan is an essential amino acid precursor of neurotransmitter serotonin and triptamine. During its metabolism, indole-3-acetic acid (IAA) is generated; this substance presents both antioxidant and prooxidant effects in different biological systems in addition to hipoglicemic effects. To date, electroencephalography (EEG) has been used to evaluate the temporal effect of several substances in neurotransmission. The goal of this study was to characterize the effect of IAA in the brain by analysing the EEG signal and evaluate the oxidative status by means of biochemical parameters. The EEG was acquired by using a noninvasive method, and the brain electric signal was analysed by advanced digital signal process- ing techniques to determinate the energy signal filtered in different band frequencies. Furthermore, the oxidative status of the brain was investi- gated by measuring the activity of antioxidant enzymes and lipid peroxidation as well as blood glucose rates of the animals treated with different doses of IAA. Our results showed the relationship of IAA administration with changes in EEG signals. The oxidative status of the brain was modified by IAA after 14days of treatment. Copyright © 2014 John Wiley & Sons, Ltd. key words—brain electrical activity; neurotransmission; IAA; oxidative stress; SOD INTRODUCTION In the mammalian brain, tryptophan is an essential amino acid precursor of neurotransmitter serotonin (5-HT). During this biosynthesis pathway, indole-3-acetic acid (IAA) is generated as a result of the monoamine oxidase-mediated oxidative deamination of triptamine. 1 Increased IAA in urine was related with disease as phenylketonuria, 2 and its teratogenic effect was observed in rats and mice. 3 The presence of peroxidase IAA acts as a prooxidant substance and generates oxidative stress by an increased formation of reactive oxygen species (ROS). 4–6 However, studies have showed that oral or subcu- taneous administration of IAA increased the phagocytic capacity of neutrophil 7 and do not have deleterious effect of rat livers 8 and mice kidneys. 9 Moreover, IAA showed potent antioxidant effects 10 and warned the mice livers against hepatocarcinoma induced by N-nitrosodietilamina (DEN). 11 To date, the effects of IAA have not yet been fully elucidated, and there have been no studies previously carried out to investigate the effect of IAA on neurotrans- mission and the oxidative status of the brain. The brain is very vulnerable to attack by ROS due to high amounts of polyunsaturated fatty acids and substances generated during metabolism that can cause damage. To defend the brain from ROS, intracellular antioxidant enzymes improve the balance during the oxidative stress and prevent degeneration. Enzymes such as superoxide dismutase (SOD), catalase (CAT) and peroxidases act as endogenous antioxidants and are used to evaluate oxidative stress. 12 In the brain, SOD is fundamental to antioxidant protective because the CAT level is low in several brain regions. 13 In addition, the level of glucose should be main- tained in the brain because oxidative stress can be generated in both hypoglicemia 14 and hyperglicemia. 15 Thus, because IAA presented both prooxidant and antioxidant effects in addition to hypoglycemic effects, in the brain, it can induce change in the oxidative status and contributes to neurode- generative disease. Reactive oxygen species are bioproducts of the cellular metabolism relationship with damage in cells and neurode- generation and determine disorders such as Parkinson’s, Alzheimer’s and Schizophrenia 16 but have a regulatory role in synaptic plasticity. 17 In this regard, electroencephalo- graphy (EEG) has been a sensitive method to evaluate the temporal response of the brain in different situations 18–23 and was recently used to characterize serotonin syndrome. 24 The EEG signal can be reliably converted into band frequen- cies and analysed in a quantitative manner. *Correspondence to: Rosana Ferrari, Department of Biological Science, State University of Santa Cruz (UESC) - Campus Soane Nazaré de Andrade, Rodovia Jorge Amado, Km 16, Bairro Salobrinho, CEP 45662–900, Ilhéus, Bahia, Brazil.E-mail: ro.ferrari74@hotmail.com Received 23 March 2014 Accepted 28 May 2014 Copyright © 2014 John Wiley & Sons, Ltd. cell biochemistry and function Cell Biochem Funct (2014) Published online in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/cbf.3043