8 research outputs found
Esquizofrenia: uma doença inflamatória?
OBJETIVO: Neste estudo, o objetivo foi revisar o papel de um possĂvel processo inflamatĂłrio na gĂȘnese da esquizofrenia. MĂTODO: Foram selecionados os trabalhos publicados em revistas indexadas nas bases de dados Lilacs e MedLine, sob os unitermos "esquizofrenia", "inflamação" e "estresse oxidativo", nos Ășltimos 10 anos atĂ© dezembro de 2009, nos idiomas inglĂȘs e portuguĂȘs. Foram excluĂdos os artigos que tratavam de aspectos fisiopatolĂłgicos da doença fora do interesse da psiquiatria. RESULTADOS: Sessenta e um artigos foram selecionados. Doze abordavam o envolvimento do estresse oxidativo na esquizofrenia, nove tratavam de alteraçÔes no sistema imunolĂłgico de pacientes esquizofrĂȘnicos, dezesseis da infecção prĂ©-natal como desencadeador da doença e sete mostravam a ação antioxidante e anti-inflamatĂłria de fĂĄrmacos antipsicĂłticos. CONCLUSĂO: Os estudos enfatizam o envolvimento do sistema imunolĂłgico (isto Ă©, interleucinas e ação anti-inflamatĂłria dos antipsicĂłticos), das infecçÔes, do estresse oxidativo e da função mitocondrial na fisiopatologia da esquizofrenia. Portanto, esses novos achados sĂŁo importantes para a melhor compreensĂŁo e, consequentemente, a elaboração de terapias mais especĂficas e eficazes no combate dessa doença mental
Oxidative Stress and Epilepsy: Literature Review
Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy. Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed. Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age
Oxidative Stress and Epilepsy: Literature Review
Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy. Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed. Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age
Monocrotaline: Histological Damage and Oxidant Activity in Brain Areas of Mice
This work was designed to study MCT effect in histopathological analysis of hippocampus (HC) and parahippocampal cortex (PHC) and in oxidative stress (OS) parameters in brain areas such as hippocampus (HC), prefrontal cortex (PFC), and striatum (ST). Swiss mice (25â30âg) were administered a single i.p. dose of MCT (5, 50, or 100âmg/kg) or 4% Tween 80 in saline (control group). After 30 minutes, the animals were sacrificed by decapitation and the brain areas (HC, PHC, PFC, or ST) were removed for histopathological analysis or dissected and homogenized for measurement of OS parameters (lipid peroxidation, nitrite, and catalase) by spectrophotometry. Histological evaluation of brain structures of rats treated with MCT (50 and 100âmg/kg) revealed lesions in the hippocampus and parahippocampal cortex compared to control. Lipid peroxidation was evident in all brain areas after administration of MCT. Nitrite/nitrate content decreased in all doses administered in HC, PFC, and ST. Catalase activity was increased in the MCT group only in HC. In conclusion, monocrotaline caused cell lesions in the hippocampus and parahippocampal cortex regions and produced oxidative stress in the HC, PFC, and ST in mice. These findings may contribute to the neurological effects associated with this compound