Lithium and valproate modulate antioxidant enzymes and prevent ouabain-induced oxidative damage in an animal model of mania

Jornada, Luciano K.; Valvassori, Samira S.; Steckert, Amanda V.; Moretti, Morgana; Mina, Francielle; Ferreira, Camila L.; Arent, Camila O.; Dal‐Pizzol, Felipe; Quevedo, João

doi:10.1016/j.jpsychires.2010.05.011

Cited by 83 publications

(49 citation statements)

References 34 publications

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“…Interestingly, there is evidence showing that oxidative stress may be increased in conditions where BDNF is described to be decreased in BD [16,17], indicating an association of BDNF and oxidative stress in BD. Furthermore, preclinical studies have shown that mood stabilizers, lithium, and valproate are able to increase BDNF levels and protect the rat brain against oxidative damage [18,19].…”

Section: Introductionmentioning

confidence: 99%

Intracerebral Administration of BDNF Protects Rat Brain Against Oxidative Stress Induced by Ouabain in an Animal Model of Mania

et al. 2014

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Several studies have suggested that alterations in brain-derived neurotrophic factor (BDNF) and increased oxidative stress have a central role in bipolar disorder (BD). Intracerebroventricular (ICV) injection of ouabain (OUA) in rats alters oxidative stress parameters and decreases BDNF levels in the brain. In this context, the present study aims to investigate the effects of BDNF ICV administration on BDNF levels and oxidative stress parameters in brains of rats submitted to animal model of mania induced by OUA. Wistar rats received an ICV injection of OUA, artificial cerebrospinal fluid (ACSF), OUA plus BDNF, or ACSF plus BDNF. Locomotor activity and risk-taking behavior in the rats were measured using the open-field test. In addition, we analyzed the BDNF levels and oxidative stress parameters (TBARS, Carbonyl, CAT, SOD, GR, and GPx) in the frontal cortex and hippocampus of rats. The BDNF was unable to reverse the ouabain-induced hyperactivity and risk-taking behavior. Nevertheless, BDNF treatment increased BDNF levels, modulated the antioxidant enzymes, and protected the OUA-induced oxidative damage in the brain of rats. These results suggest that BDNF alteration observed in BD patients may be associated with oxidative damage, both seen in this disorder.

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Section: Introductionmentioning

confidence: 99%

Intracerebral Administration of BDNF Protects Rat Brain Against Oxidative Stress Induced by Ouabain in an Animal Model of Mania

et al. 2014

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“…Interestingly, lithium and VPA were able to protect the brain against the protein and lipid damage and SOD and CAT changes induced by OUA in rats. 156 Machado-Vieira et al 160 demonstrated an increase of lipid damage in the plasma of BD patients during initial episodes of mania, when compared with healthy controls. This study also reported an increase of SOD and CAT, which are natural antioxidant defenses.…”

Section: Animal Models Of Bipolar Disordermentioning

confidence: 98%

“…154,156 Moreover, it has been shown that activity of the enzymes catalase (CAT) and superoxide dismutase (SOD) is altered in the brain and cerebrospinal fluid of rats subjected to the animal model of mania induced by OUA. [156][157][158][159] Brocardo et al 157 also demonstrated that glutathione peroxidase and glutathione reductase levels are decreased in the hippocampus and cortex of rats after ICV OUA injection. Interestingly, lithium and VPA were able to protect the brain against the protein and lipid damage and SOD and CAT changes induced by OUA in rats.…”

Section: Animal Models Of Bipolar Disordermentioning

confidence: 99%

Contributions of animal models to the study of mood disorders

Valvassori

Budni

Varela

et al. 2013

Rev. Bras. Psiquiatr.

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Mood disorders are a leading cause of morbidity and mortality, yet their underlying pathophysiology remains unclear. Animal models serve as a powerful tool for investigating the neurobiological mechanisms underlying psychiatric disorders; however, no animal model developed to date can fully mimic the ''corresponding'' human psychiatric disorder. In this scenario, the development of different animal models contributes to our understanding of the neurobiology of these disorders and provides the possibility of preclinical pharmacologic screening. The present review seeks to provide a comprehensive overview of traditional and recent animal models, recapitulating different features and the possible pathologic mechanisms of mood disorders emulated by these models.

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“…Administration of N-acetyl-cysteine (NAC), which is a precursor of glutathione, has been associated with improved short-term spatial memory in rats and with depression in humans (Choy et al, 2010;Magalhaes et al, 2011). Moreover, antioxidant effects of mood stabilizers including lithium and valproic acid have been observed in animal models of oxidant-induced mania (Jornada et al, 2011). These findings further support the role of oxidative stress in bipolar disorders while emphasizing the protective effects of mood stabilizers with regard to their proposed antioxidant effects on the brain.…”

Section: The Role Of Oxidative Stressmentioning

confidence: 99%