@article{ref1,
title="Creatine reduces oxidative stress markers but does not protect against seizure susceptibility after severe traumatic brain injury",
journal="Brain research bulletin",
year="2012",
author="Saraiva, André Luis Lopes and Ferreira, Ana Paula Oliveira and Silva, Luiz Fernando Almeida and Hoffmann, Maurício Scopel and Dutra, Fabrício Diniz and Furian, Ana Flávia and Oliveira, Mauro Schneider and Fighera, Michele Rechia and Royes, Luiz Fernando Freire",
volume="87",
number="2-3",
pages="180-186",
abstract="Achievements made over the last years have highlighted the important role of creatine in health and disease. However, its effects on hyperexcitable circuit and oxidative damage induced by traumatic brain injury (TBI) are not well understood. In the present study we revealed that severe TBI elicited by fluid percussion brain injury induced oxidative damage characterized by protein carbonylation, thiobarbituric acid reactive species (TBARS) increase and Na(+),K(+)-ATPase activity inhibition 4 and 8 days after neuronal injury. Statistical analysis showed that after TBI creatine supplementation (300mg/kg, p.o.) decreased the levels of protein carbonyl and TBARS but did not protect against TBI-induced Na(+),K(+)-ATPase activity inhibition. Electroencephalography (EEG) analysis revealed that the injection of a subconvulsant dose of PTZ (35mg/kg, i.p.), 4 but not 8 days after neuronal injury, decreased latency for the first clonic seizures and increased the time of spent generalized tonic-clonic seizures compared with the sham group. In addition, creatine supplementation had no effect on convulsive parameters induced by a subconvulsant dose of PTZ. Current experiments provide evidence that lipid and protein oxidation represents a separate pathway in the early post-traumatic seizures susceptibility. Furthermore, the lack of consistent anticonvulsant effect exerted by creatine in this early phase suggests that its apparent antioxidant effect does not protect against excitatory input generation induced by TBI.<p /> <p>Language: en</p>",
language="en",
issn="0361-9230",
doi="10.1016/j.brainresbull.2011.10.010",
url="http://dx.doi.org/10.1016/j.brainresbull.2011.10.010"
}