Anacardic Acids from Cashew Nuts Prevent Behavioral Changes and Oxidative Stress Induced by Rotenone in a Rat Model of Parkinson’s Disease

Autor:	Almir Gonçalves Wanderley, Ricielle Lopes Augusto, Adriana Sereniki, Simone S.L. Lafayette, Glauber Rudá Feitoza Braz, Renata de Cássia Ribas Perreira, Soraya S. Smailli, Francisco Thiago Correia de Souza, Belmira Lara da Silveira Andrade-da-Costa, Cybelle Façanha Barreto Medeiros-Linard, Ivone Antônia de Souza, Claudia Jacques Lagranha, M. T. S. Trevisan
Rok vydání:	2018
Předmět:	Male 0301 basic medicine Insecticides Antioxidant Parkinson's disease medicine.medical_treatment Substantia nigra Pharmacology Toxicology medicine.disease_cause Neuroprotection Antioxidants Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Rotenone Animals Medicine Rats Wistar Maze Learning biology Superoxide Dismutase business.industry Mental Disorders General Neuroscience Brain Parkinson Disease medicine.disease Anacardic Acids Rats Anacardic acids Disease Models Animal Oxidative Stress 030104 developmental biology Electron Transport Chain Complex Proteins chemistry Rotarod Performance Test Exploratory Behavior biology.protein Lipid Peroxidation business Locomotion 030217 neurology & neurosurgery Oxidative stress
Zdroj:	Neurotoxicity Research. 34:250-262
ISSN:	1476-3524 1029-8428
DOI:	10.1007/s12640-018-9882-6
Popis:	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.
Databáze:	OpenAIRE
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