Effect of N-acetylcysteine and/or deferoxamine on oxidative stress and hyperactivity in an animal model of mania

Valvassori, Samira S.; Petronilho, Fabrícia; Réus, Gislaine Z.; Steckert, Amanda V.; Oliveira, Virgínia B.M.; Boeck, Carina Rodrigues; Kapczinski, Flávio; Dal‐Pizzol, Felipe; Quevedo, Joao L De

doi:10.1016/j.pnpbp.2008.02.012

Cited by 42 publications

(22 citation statements)

References 45 publications

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“…The present findings are in agreement with our previous results indicating that AMPH treatment induces hyperlocomotion (Frey et al 2006a, b, c, d, e, f;Kauer-Sant'Anna et al 2007;Correa et al 2007;Valvassori et al 2008;Andreazza et al 2008;Streck et al 2008;Zugno et al 2009). Here, as in our previous study using this two-hit animal model of mania (De Lima et al 2011), we demonstrated that the hyperlocomotion is accompanied by severe memory impairments, which persist at least for 8 days after the last AMPH injection in both ND and D groups.…”

Section: Discussionsupporting

confidence: 94%

“…VPA 200 mg/kg) and one injection in the afternoon (VPA 200 mg/ kg). The doses of AMPH and VPA were selected on the basis of previous studies from our laboratories (Frey et al 2006a, b, c, d, e, f;Correa et al 2007;Valvassori et al 2008;Walz et al 2008;Andreazza et al 2008;Streck et al 2008;Zugno et al 2009;De Lima et al 2011). Drugs were prepared freshly before each experiment.…”

Section: Treatmentsmentioning

confidence: 99%

“…We have shown that brain oxidative stress (Frey et al 2006a, c, f;Valvassori et al 2008), neurotrophic factors' levels [brainderived neurotrophic factor (BDNF), nerve growth factor (NGF) and neurotrophin-3 (NT-3)] (Frey et al 2006d, e;Walz et al 2008), DNA damage , creatine kinase activity (Streck et al 2008), and Na ? ,K ?…”

Section: Introductionmentioning

confidence: 99%

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Early life stress exacerbates cognitive dysfunction induced by d-amphetamine: amelioration by valproic acid

et al. 2012

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It has been demonstrated that experiences taking place early in life have a profound influence on brain development, interacting with the genetic background and determining differences in the vulnerability to the onset of bipolar disorder when the individual is exposed to a second adverse event later in life. Here, we investigated the effects of exposure to an early adverse life event (maternal deprivation) and to a later adverse life event [D-amphetamine (AMPH)] on cognition in an animal model of mania. We have previously demonstrated that that repeated AMPH exposure produces severe and persistent cognitive impairment, which was more pronounced when the animals were maternal deprived, suggesting that the early adverse life event could be potentiating the effects of the exposure to the second adverse life event later in life. Here, we show that valproic acid ameliorated the cognitive deficits induced by AMPH, but it was not effective when the animals were exposed to both stressors: maternal deprivation and AMPH treatment.

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Section: Discussionsupporting

confidence: 94%

Section: Treatmentsmentioning

confidence: 99%

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Early life stress exacerbates cognitive dysfunction induced by d-amphetamine: amelioration by valproic acid

et al. 2012

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“…Many studies have revealed that brain energetic metabolism impairment may be involved in mood disorders (Jou et al 2009;Lucca et al 2009;Rezin et al 2009a;Streck et al 2008;Valvassori et al 2008;Corrêa et al 2007;Konradi et al 2004;Kato and Kato 2000). The enzyme creatine kinase (EC 2.7.3.2) is crucial for highenergy-consuming tissues, such as, brain, which works as a buffering system of cellular adenosine triphosphate (ATP) levels (Bessman and Carpenter 1985).…”

Section: Introductionmentioning

confidence: 99%

Administration of memantine and imipramine alters mitochondrial respiratory chain and creatine kinase activities in rat brain

et al. 2011

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Several studies have appointed for a role of glutamatergic system and/or mitochondrial function in major depression. In the present study, we evaluated the creatine kinase and mitochondrial respiratory chain activities after acute and chronic treatments with memantine (N-methyl-D: -aspartate receptor antagonist) and imipramine (tricyclic antidepressant) in rats. To this aim, rats were acutely or chronically treated for 14 days once a day with saline, memantine (5, 10 and 20 mg/kg) and imipramine (10, 20 and 30 mg/kg). After acute or chronic treatments, we evaluated mitochondrial respiratory chain complexes (I, II, II-III and IV) and creatine kinase activities in prefrontal cortex, hippocampus and striatum. Our results showed that both acute and chronic treatments with memantine or imipramine altered respiratory chain complexes and creatine kinase activities in rat brain; however, these alterations were different with relation to protocols (acute or chronic), complex, dose and brain area. Finally, these findings further support the hypothesis that the effects of imipramine and memantine could be involve mitochondrial function modulation.

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“…Os modelos animais de mania efetivamente mostram desbalanço na biologia oxidativa [66][67][68][69][70][71] . Estudos clínicos indicam alto dano oxidativo sistêmico em pacientes com transtorno bipolar [72][73][74][75][76] .…”

Section: Estresse Oxidativounclassified

Marcadores periféricos e a fisiopatologia do transtorno bipolar

Magalhães¹,

Fries²,

Kapczinski³

2012

Rev. psiquiatr. clín.

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Introdução: O entendimento da fisiopatologia do transtorno bipolar vem tendo avanços consistentes nos últimos anos. Um enfoque na relação entre carga alostática e alterações sistêmicas vem tomando corpo, com o objetivo de se entender a frequente progressão da doença. Proeminentes entre os mediadores periféricos têm sido as moléculas que poderiam ser amplamente agrupadas em neurotrofinas, marcadores de estresse oxidativo e marcadores inflamatórios. Objetivo: Descrever achados recentes em relação à fisiopatologia sistêmica do transtorno bipolar, com enfoque especial em estudos brasileiros, tentando articular uma visão coerente do conhecimento atual do campo. Método: Revisão narrativa da literatura relacionada a neurotrofinas, estresse oxidativo e marcadores inflamatórios no transtorno bipolar. Resultados: Diversas fontes de evidência, provenientes tanto de estudos pré-clínicos quanto clínicos, revelam consistentemente alterações sistêmicas no transtorno bipolar. Os achados são especialmente robustos em pacientes com múltiplos episódios. Nesses, alterações relacionadas a episódios de mania e depressão são notáveis em neurotrofinas e dano oxidativo a lipídeos. Um número menor de estudos mostra alterações no sistema imune, em particular estados pró-inflamatórios. Conclusão: Alterações sistêmicas que correlacionam o transtorno bipolar a comorbidade clínica, disfunção cognitiva, incapacidade e mortalidade precoce começam a ser traçadas. Estudos envolvendo desenhos longitudinais, amostras populacionais e ensaios clínicos envolvendo marcadores periféricos devem ser incorporados no futuro próximo e reforçar a validade de uma noção de envolvimento multissistêmico no transtorno bipolar.Magalhães PVS, et al. / Rev Psiq Clín. 2012;39(2):60-7 Palavras-chave: Transtorno bipolar, inflamação, estresse oxidativo, neurotrofinas, fator neurotrófico derivado do cérebro, fisiopatologia, biomarcadores. ABSTRACT Introduction:The understanding of the pathophysiology of bipolar disorder has steadily advanced in the past few years. Thereby, a focus on allostatic load and systemic changes has appeared, with the aim to understand illness progression. Amongst the peripheral markers, molecules that can be widely classified into neurotrophins, oxidadive stress markers, and inflammation markers have been elevated. Objective: To describe recent findings regarding the systemic pathophysiology of bipolar disorder, with a special focus on Brazilian studies and to create a coherent view of the current knowledge in the field. Method: Narrative review of the literature regarding neurotrophins, oxidative stress, and inflammatory markers in bipolar disorder. Results: A diverse body of evidence, based on both pre-clinical and clinical studies, reveals consistent systemic changes in bipolar disorder. The findings are particularly robust in patients after multiple episodes. Thereby, remarkable changes related to manic and depressive episodes were found in neurotrophins and oxidative damage to lipids. Regarding to immune system alterations, in particular pro...

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Effect of N-acetylcysteine and/or deferoxamine on oxidative stress and hyperactivity in an animal model of mania

Cited by 42 publications

References 45 publications

Early life stress exacerbates cognitive dysfunction induced by d-amphetamine: amelioration by valproic acid

Early life stress exacerbates cognitive dysfunction induced by d-amphetamine: amelioration by valproic acid

Administration of memantine and imipramine alters mitochondrial respiratory chain and creatine kinase activities in rat brain

Marcadores periféricos e a fisiopatologia do transtorno bipolar

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