α-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression

Lobato, Kelly R.; Cardoso, Chandra Chiappin; Binfaré, Ricardo W.; Budni, Josiane; Wagner, Cristiane L.R.; Brocardo, Patrícia S.; Souza, Luiz Felipe de; Brocardo, Caroline; Flesch, Samira; Freitas, Andiara E.; Dafré, Alcir Luiz; Rodrigues, Ana Lúcia S.

doi:10.1016/j.bbr.2010.02.002

Cited by 60 publications

(38 citation statements)

References 59 publications

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“…These findings corroborate with the behavioral results presented here and with previous studies from our group that showed the reversal effect of ALA on the depressivelike behavior of animals treated with CORT (Silva et al, , 2014. Furthermore, several studies show that antioxidants are able to reverse depressive-like behavior alone or in association with antidepressants (Lobato et al, 2010;Moretti et al, 2012;Mazloom et al, 2013;Manosso et al, 2013;Amr et al, 2013).…”

Section: Discussionsupporting

confidence: 95%

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Sousa

Meneses

Vasconcelos

et al. 2015

Psychiatry Research

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Brain derived neurotrophic factor (BDNF) is linked to the pathophysiology of depression. We hypothesized that BDNF is one of the neurobiological pathways related to the augmentation effect of alpha-lipoic acid (ALA) when associated with antidepressants. Female mice were administered vehicle or CORT 20mg/kg during 14 days. From the 15th to 21st days the animals were divided in groups that were further administered: vehicle, desvenlafaxine (DVS) 10 or 20mg/kg, ALA 100 or 200mg/kg or the combinations of DVS10+ALA100, DVS20+ALA100, DVS10+ALA200 or DVS20+ALA200. ALA or DVS alone or in combination reversed CORT-induced increase in immobility time in the forced swimming test and decrease in sucrose preference, presenting, thus, an antidepressant-like effect. DVS10 alone reversed CORT-induced decrease in BDNF in the prefrontal cortex (PFC), hippocampus (HC) and striatum (ST). The same was observed in the HC and ST of ALA200 treated animals. The combination of DVS and ALA200 reversed CORT-induced alterations in BDNF and even, in some cases, increased the levels of this neurotrophin when compared to vehicle-treated animals in HC and ST. Taken together, these results suggest that the combination of the DVS+ALA may be valuable for treating conditions in which BDNF levels are decreased, such as depression.

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Section: Discussionsupporting

confidence: 95%

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Sousa

Meneses

Vasconcelos

et al. 2015

Psychiatry Research

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“…Indeed, several antioxidant compounds have been reported to present antidepressant properties (Aboul-Fotouh, 2013;Lobato et al, 2010;Srinivasan et al, 2012), including GSH (Rosa et al, 2013). Although alterations in GSH levels in depressive subjects were found (Kodydkova et al, 2009;Rybka et al, 2013), in our study none of the groups presented any significant alteration in the hippocampal levels of this antioxidant.…”

Section: Discussioncontrasting

confidence: 78%

Guanosine prevents behavioral alterations in the forced swimming test and hippocampal oxidative damage induced by acute restraint stress

Bettio

Freitas

Neis

et al. 2014

Pharmacology Biochemistry and Behavior

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Guanosine is a guanine-based purine that modulates glutamate uptake and exerts neurotrophic and neuroprotective effects. In a previous study, our group demonstrated that this endogenous nucleoside displays antidepressant-like properties in a predictive animal model. Based on the role of oxidative stress in modulating depressive disorders as well as on the association between the neuroprotective and antioxidant properties of guanosine, here we investigated if its antidepressant-like effect is accompanied by a modulation of hippocampal oxidant/antioxidant parameters. Adult Swiss mice were submitted to an acute restraint stress protocol, which is known to cause behavioral changes that are associated with neuronal oxidative damage. Animals submitted to ARS exhibited an increased immobility time in the forced swimming test (FST) and the administration of guanosine (5mg/kg, p.o.) or fluoxetine (10mg/kg, p.o., positive control) before the exposure to stressor prevented this alteration. Moreover, the significantly increased levels of hippocampal malondialdehyde (MDA; an indicator of lipid peroxidation), induced by ARS were not observed in stressed mice treated with guanosine. Although no changes were found in the hippocampal levels of reduced glutathione (GSH), the group submitted to ARS procedure presented enhanced glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) activities and reduced catalase (CAT) activity in the hippocampus. Guanosine was able to prevent the alterations in GPx, GR, CAT activities, and in SOD/CAT activity ratio, but potentiated the increase in SOD activity elicited by ARS. Altogether, the present findings indicate that the observed antidepressant-like effects of guanosine might be related, at least in part, to its capability of modulating antioxidant defenses and mitigating hippocampal oxidative damage induced by ARS.

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“…Moreover, some of the neurological symptoms of vitamin E deficiency, like the increased permeability of capillaries during encephalomalacia in the chick, could be the result of impaired formation of a vascular network and deficient barrier function in the brain [127]. The antidepressant-like effects observed with aT or aTP treatment [128] could also be explained by induction of VEGF [129].…”

Section: Possible Implicationsmentioning

confidence: 96%

α‐Tocopheryl phosphate—An activated form of vitamin E important for angiogenesis and vasculogenesis?

2012

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Vitamin E was originally discovered as a dietary factor essential for reproduction in rats. Since then, vitamin E has revealed many important molecular properties such as the scavenging of reactive oxygen and nitrogen species or the modulation of signal transduction and gene expression in antioxidant and nonantioxidant manners. A congenital disease, ataxia with vitamin E deficiency, which is characterized by impaired enrichment of α-tocopherol (αT) in plasma due to mutations in the α-tocopherol transfer protein gene, has been discovered. An effect of vitamin E on angiogenesis and vasculogenesis has been observed in several studies, and recently, it has been demonstrated in the placenta of pregnant ewes, possibly involving the stimulation of vascular endothelial growth factor (VEGF) expression. We recently observed that the phosphorylated form of αT, α-tocopheryl phosphate (αTP), increases the expression of VEGF. We propose that the stimulatory effect of αT on angiogenesis and vasculogenesis is potentiated by phosphorylation to αTP, which may act as a cofactor or active lipid mediator increasing VEGF expression. Increased VEGF expression and consequent enhanced angiogenesis and vasculogenesis induced by αTP may explain not only the essential roles of vitamin E on reproduction, but also its beneficial effects against pre-eclampsia, ischemia/reperfusion injury, and during wound healing. It may also serve as a survival factor for brain and muscle cells. The finding that αTP may regulate vasculogenesis may indicate potential, important pathophysiological implications.

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α-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression

Cited by 60 publications

References 59 publications

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Guanosine prevents behavioral alterations in the forced swimming test and hippocampal oxidative damage induced by acute restraint stress

α‐Tocopheryl phosphate—An activated form of vitamin E important for angiogenesis and vasculogenesis?

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