Antioxidant activity elicited by low dose of caffeine attenuates pentylenetetrazol-induced seizures and oxidative damage in rats |
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Authors: | Mauren Assis Souza Bibiana Castagna Mota Rogério Rosa Gerbatin Fernanda Silva Rodrigues Mauro Castro Michele Rechia Fighera Luiz Fernando Freire Royes |
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Institution: | 1. Programa de Pós-graduação em Ciências Biológicas, Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Brazil;2. Laboratório de Bioquímica do Exercício, Centro de Educação Física e Desportos., Universidade Federal de Santa Maria, Santa Maria, RS, Brazil;3. Programa de Pós-graduação em Farmacologia, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil;4. Departamento de Métodos e Técnicas Desportivas., Universidade Federal de Santa Maria, Santa Maria, RS, Brazil;5. Departamento de Neuropsiquiatria, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil |
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Abstract: | Although caffeine supplementation has a beneficial effect on people with neurological disorders, its implications for oxidative damage related to seizures are not well documented. Thus the aim of this study was to investigate the effects of two weeks caffeine supplementation (6 mg/kg; p.o.) on seizures and neurochemical alterations induced by pentylenetetrazol (PTZ 60 mg/kg i.p.). Statistical analyses showed that long-term rather than single dose caffeine administration decreased the duration of PTZ-induced seizures in adult male Wistar rats as recorded by cortical electroencephalographic (EEG) and behavioral analysis. The quantification of EEG recordings also revealed that caffeine supplementation protected against a wave increase induced by PTZ. Neurochemical analyses revealed that caffeine supplementation increased glutathione (GSH) content per se and protected against the increase in the levels of thiobarbituric acid reactive substances (TBARS) and oxidized diclorofluoresceine diacetate (DCFH-DA). Also, caffeine prevent the decrease in GSH content and Na+, K+-ATPase activity induced by PTZ. Our data also showed that the infusion of L-buthionine sulfoximine (BSO; 3.2 μmol/site i.c.v), an inhibitor of GSH synthesis, two days before injecting PTZ reversed the anticonvulsant effect caused by caffeine. BSO infusion also decreased GSH content and Na+, K+-ATPase activity. However, it increased DCFH-DA oxidation and TBARS per se and reversed the protective effect of caffeine. Results presented in this paper support the neuroprotective effects of low long-term caffeine exposure to epileptic damage and suggest that the increase in the cerebral GSH content caused by caffeine supplementation may provide a new therapeutic approach to the control of seizure. |
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Keywords: | Caffeine Seizures Oxidative damage GSH Na+ K+-ATPase activity BSO |
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