Antidepressant-like activity of zinc: further behavioral and molecular evidence

Sowa-Kućma, Magdalena; Legutko, Beata; Szewczyk, Bernadeta; Novak, Kinga; Znojek, Paweł; Poleszak, Ewa; Papp, Mariusz; Pilc, Andrzej; Nowak, Gabriel

doi:10.1007/s00702-008-0115-7

Cited by 113 publications

(72 citation statements)

References 36 publications

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“…There is some evidence coming from preclinical and clinical studies suggesting a relationship between dietary zinc intake and depressive symptoms [5,29,64,68,69]. Zinc shows antidepressant-like properties in preclinical test and models [6,10,20,21,36,42,52]. Recently, there has been emerging evidence that zinc deficiency can induce depressive-like behavior in mice [30,31,69] and rats [57,64,67].…”

Section: Introductionmentioning

confidence: 99%

Zinc deficiency alters responsiveness to antidepressant drugs in mice

Młyniec

Budziszewska

Reczyński

et al. 2013

Pharmacological Reports

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Abstract:Background: There is some evidence coming from preclinical and clinical studies suggesting a relationship between dietary zinc intake and depressive symptoms. The aim of the study was to determine whether zinc deficiency alters the response to antidepressants with a different mechanism of action. We examine also whether these changes are related to activity of the hypothalamic-pituitaryadrenal HPA axis. Methods: Male CD-1 mice were assigned to groups according to diet and antidepressant administration. To evaluate animal behavior, the immobility time in the forced swim test (FST) and locomotor activity were measured. To determine serum zinc levels the flame atomic absorption spectroscopy (FAAS) was used. The serum corticosterone was determined by radioimmunoassay (RIA). Results: Antidepressants administered to zinc-deprived mice induced an altered response in the FST when compared to animals fed with an adequate diet. There were no changes in locomotor activity. Animals subjected to a zinc-deficient diet showed a significant reduction in serum zinc levels, which was normalized by antidepressant treatment. An increase in serum corticosterone concentrations in mice fed with a zinc-deficient diet and treated with antidepressants was observed, so it can be concluded that reduced levels of zinc contribute hyperactivation of the HPA axis. Conclusion:The results of this study suggest that a diet with a reduced zinc level alters antidepressant action, which is associated with a reduction in the serum zinc level and rise in the corticosterone level. The results of this study may indicate the involvement of zinc deficiency in the pathogenesis of depression.

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Section: Introductionmentioning

confidence: 99%

Zinc deficiency alters responsiveness to antidepressant drugs in mice

Młyniec

Budziszewska

Reczyński

et al. 2013

Pharmacological Reports

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“…Moreover, recent studies have demonstrated that zinc (as hydroaspartate salt) in single, subchronic or chronic administration reduced the immobility time in different animal models of depression (as olfactory bulbectomy, chronic mild, stress, chronic unpredictable stress and forced swimming test) 32,33 . The results showed, to our knowledge for the first time, that ZnCl 2 (30 mg/kg) after chronic administration is effective in reducing the immobility time in the FST, consistent with an antidepressant effect in this predictive test 34 .…”

Section: Discussionmentioning

confidence: 99%

Biological activities of Zn(II)-S-methyl-cysteine complex as antiradical, inhibitor of acid phosphatase enzyme and in vivo antidepressant effects

Escudero¹,

Martini

Jori

et al. 2016

Journal of Enzyme Inhibition and Medicinal Chemistry

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The antidepressant effect of simple Zn(II) salts has been proved in several animal models of depression. In this study, a coordination metal complex of Zn(II) having a sulfur containing ligand is tested as antidepressant for the first time. Forced swimming test method on male Wistar rats shows a decrease in the immobility and an increase in the swimming behavior after treatment with [Zn(S-Met) 2 ] (S-Met¼S-methyl-L-cysteine) being more effective and remarkable than ZnCl 2 . The thiobarbituric acid and the pyranine consumption (hydroxyl and peroxyl radicals, respectively) methods were applied to evaluate the antioxidant activity of S-Met and [Zn(S-Met) 2 ] showing evidence of attenuation of hydroxyl but not peroxyl radicals activities. UVvis studies on the inhibition of acid phosphatase enzyme (AcP) demonstrated that S-methyl-Lcysteine did not produce any effect but, in contrast, [Zn(S-Met) 2 ] complex behaved as a moderate inhibitor. Finally, bioavailability studies were performed by fluorescence spectroscopy denoting the ability of the albumin to transport the complex.

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“…However, no animal study or clinical trial has tested the therapeutic potential of zinc sulfate in HD. Recently, Sowa-Kuma and colleagues 10 tested the antidepressant activity of zinc hydroaspartate in an animal model of depression and the effect of zinc treatment on BDNF protein and the mRNA level. They found zinc hydroaspartate exhibited a rapid antidepressant-like effect and zinc treatment induced a 17% to 39% increase in the BDNF mRNA and protein level in the hippocampus.…”

Section: To the Editor: July 31 2009mentioning

confidence: 99%

Zinc Sulfate Could be a Potential Agent for the Treatment of Huntington's Disease Through Activating Central TrkB Signaling

Wu¹

2010

CNS Spectr.

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Antidepressant-like activity of zinc: further behavioral and molecular evidence

Cited by 113 publications

References 36 publications

Zinc deficiency alters responsiveness to antidepressant drugs in mice

Zinc deficiency alters responsiveness to antidepressant drugs in mice

Biological activities of Zn(II)-S-methyl-cysteine complex as antiradical, inhibitor of acid phosphatase enzyme and in vivo antidepressant effects

Zinc Sulfate Could be a Potential Agent for the Treatment of Huntington's Disease Through Activating Central TrkB Signaling

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