ORIGINAL ARTICLE Anacardic Acids from Cashew Nuts Prevent Behavioral Changes and Oxidative Stress Induced by Rotenone in a Rat Model of Parkinson’s Disease Cybelle Façanha Barreto Medeiros-Linard 1 & Belmira Lara da Silveira Andrade-da-Costa 1 & Ricielle Lopes Augusto 1 & Adriana Sereniki 1 & Maria Teresa Sales Trevisan 2 & Renata de Cássia Ribas Perreira 1 & Francisco Thiago Correia de Souza 2 & Glauber Ruda Feitoza Braz 3 & Claudia Jacques Lagranha 3 & Ivone Antônia de Souza 4 & Almir Gonçalves Wanderley 1 & Soraya S. Smailli 5 & Simone Sette Lopes Lafayette 1 Received: 22 April 2017 /Revised: 12 February 2018 /Accepted: 14 February 2018 # Springer Science+Business Media, LLC, part of Springer Nature 2018 Abstract Anacardic acids (AAs) are alkyl phenols mainly presenting in cashew nuts. The antioxidant effects of these compounds have been an area of interest in recent research, with findings suggesting potential therapeutic use for certain diseases. Nevertheless, none of these studies were performed in order to test the hypothesis of whether anacardic acids are capable of preventing behavioral changes and oxidative stress induced by the pesticide rotenone in experimental model of Parkinson’ s disease. In our research, adult male rats were treated orally with AAs (1, 3, 10, 25, 50, or 100 mg/kg/day) 1 h before rotenone (3 mg/kg; s.c.) for five consecutive days. The behavioral testing strategies, including tests for general locomotor activity (open field), motor coordination (rotarod), and spatial memory performance (elevated T-maze), were carried out. Lipoperoxidation levels and total superoxide dismutase (t-SOD) activity, as well as cytoplasmic and mitochondrial SOD gene expression, were assessed in the substantia nigra (SN), striatum, and cerebral cortex. The results showed that AAs dose-dependently prevented the rotenone-induced learning and motor impairment from 10 mg/kg/day. AAs also precluded rotenone-induced lipoperoxidation in all doses, acting directly on the mitochondria, and improved the t-SOD activity in the doses 25–100 mg/kg/day. AAs per se (100 mg/kg/day) increased SOD gene expression and t-SOD activity. Our findings indicate that the oral administration of AAs prevents rotenone-induced behavioral changes and oxidative stress, in part due to a modulatory action on the mitochondria and SOD gene expression. These data suggest that AAs have promising neuroprotective action against degenerative changes in Parkinson’ s disease. Keywords Rotenone . Lipoperoxidation . Superoxide dismutase . Substantia nigra . Motor behavior Introduction Parkinson’ s disease (PD) is a prevalent neurodegenerative dis- order characterized by motor, limbic and cognitive impairment that negatively affects the quality of life during aging (Jankovic 2008; de Farias et al. 2016). Population-based stud- ies have indicated that the number of individuals looking for treatment for PD is likely to increase significantly over the Cybelle Façanha Barreto Medeiros-Linard, Belmira Lara da Silveira Andrade-da-Costa and Ricielle Lopes Augusto contributed equally to this work. * Simone Sette Lopes Lafayette simonesette@terra.com.br 1 Departamento de Fisiologia e Farmacologia, Centro de Biociências, Universidade Federal de Pernambuco, Av. da Engenharia, s/n, Cidade Universitária, Recife, Pernambuco CEP 50740600, Brazil 2 Departamento de Química Orgânica e Inorgânica, Universidade Federal do Ceará, Fortaleza, CE, Brazil 3 Laboratorio de Bioquimica e Bioquímica do Exercício, Centro Acadêmico de Vitória da Universidade Federal de Pernambuco, Vitória de Santo Antão, Brazil 4 Departamento de Farmacologia, Universidade Federal de São Paulo, São Paulo, SP, Brazil 5 Departamento de Antibióticos, Universidade Federal de Pernambuco, Recife, Brazil Neurotoxicity Research https://doi.org/10.1007/s12640-018-9882-6