Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

• Autor(a) principal: Koohsari,Motahareh
• Data de Publicação: 2016
• Outros Autores: Shaki,Fatemeh, Jahani,Daniel
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Brazilian Archives of Biology and Technology
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132016000100342
• topic: Edaravone; Methamphetamine; cardiotoxicity; Oxidative stress; Mitochondria

ABSTRACT Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METH-induced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.