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Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice

The overexposure to nickel due to the extensive use of it in modern technology remains a major public health concern. The mechanisms of pathological effects of this metal remain elusive. The present study was devoted to evaluate the effect of nickel on the oxidative state of the brain cells of mice...

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Autores principales: Šulinskienė, Jurgita, Bernotienė, Rasa, Baranauskienė, Dalė, Naginienė, Rima, Stanevičienė, Inga, Kašauskas, Artūras, Ivanov, Leonid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6745131/
https://www.ncbi.nlm.nih.gov/pubmed/31565155
http://dx.doi.org/10.1155/2019/8549727
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author Šulinskienė, Jurgita
Bernotienė, Rasa
Baranauskienė, Dalė
Naginienė, Rima
Stanevičienė, Inga
Kašauskas, Artūras
Ivanov, Leonid
author_facet Šulinskienė, Jurgita
Bernotienė, Rasa
Baranauskienė, Dalė
Naginienė, Rima
Stanevičienė, Inga
Kašauskas, Artūras
Ivanov, Leonid
author_sort Šulinskienė, Jurgita
collection PubMed
description The overexposure to nickel due to the extensive use of it in modern technology remains a major public health concern. The mechanisms of pathological effects of this metal remain elusive. The present study was devoted to evaluate the effect of nickel on the oxidative state of the brain cells of mice and to assess whether zinc as redox state modulator could efficiently protect cells against nickel's neurotoxicity. As oxidative stress biomarkers in the present study, we have measured the concentrations of reduced glutathione, metallothioneins, and malondialdehyde and the activity of the enzyme δ-aminolevulinate dehydratase. For the single metal exposure, mice were i.p. injected once with solutions of NiCl(2) and/or ZnSO(4); repeated exposure was performed i.p. injecting metal salt solutions for 14 days (once a day). The control mice received i.p. injections of saline. Results of our study demonstrate that single and 14 days of Ni(2+) exposure decreased reduced glutathione and increased malondialdehyde contents in the brain of mice. Repeated Ni(2+) administration significantly inhibited δ-aminolevulinate dehydratase while increasing brain metallothionein concentration at both exposure periods. Zinc exhibited a protective effect against nickel-induced glutathione and lipid peroxidation in brain cells of mice at both intervals of time, while repeated exposure to this metal significantly raised the brain metallothionein content. Repeated Zn(2+) pretreatment protected δ-aminolevulinate dehydratase from Ni(2+)-induced inhibition and significantly increased metallothionein concentration at both investigated time intervals.
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spelling pubmed-67451312019-09-29 Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice Šulinskienė, Jurgita Bernotienė, Rasa Baranauskienė, Dalė Naginienė, Rima Stanevičienė, Inga Kašauskas, Artūras Ivanov, Leonid Oxid Med Cell Longev Research Article The overexposure to nickel due to the extensive use of it in modern technology remains a major public health concern. The mechanisms of pathological effects of this metal remain elusive. The present study was devoted to evaluate the effect of nickel on the oxidative state of the brain cells of mice and to assess whether zinc as redox state modulator could efficiently protect cells against nickel's neurotoxicity. As oxidative stress biomarkers in the present study, we have measured the concentrations of reduced glutathione, metallothioneins, and malondialdehyde and the activity of the enzyme δ-aminolevulinate dehydratase. For the single metal exposure, mice were i.p. injected once with solutions of NiCl(2) and/or ZnSO(4); repeated exposure was performed i.p. injecting metal salt solutions for 14 days (once a day). The control mice received i.p. injections of saline. Results of our study demonstrate that single and 14 days of Ni(2+) exposure decreased reduced glutathione and increased malondialdehyde contents in the brain of mice. Repeated Ni(2+) administration significantly inhibited δ-aminolevulinate dehydratase while increasing brain metallothionein concentration at both exposure periods. Zinc exhibited a protective effect against nickel-induced glutathione and lipid peroxidation in brain cells of mice at both intervals of time, while repeated exposure to this metal significantly raised the brain metallothionein content. Repeated Zn(2+) pretreatment protected δ-aminolevulinate dehydratase from Ni(2+)-induced inhibition and significantly increased metallothionein concentration at both investigated time intervals. Hindawi 2019-09-02 /pmc/articles/PMC6745131/ /pubmed/31565155 http://dx.doi.org/10.1155/2019/8549727 Text en Copyright © 2019 Jurgita Šulinskienė et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Šulinskienė, Jurgita
Bernotienė, Rasa
Baranauskienė, Dalė
Naginienė, Rima
Stanevičienė, Inga
Kašauskas, Artūras
Ivanov, Leonid
Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice
title Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice
title_full Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice
title_fullStr Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice
title_full_unstemmed Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice
title_short Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice
title_sort effect of zinc on the oxidative stress biomarkers in the brain of nickel-treated mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6745131/
https://www.ncbi.nlm.nih.gov/pubmed/31565155
http://dx.doi.org/10.1155/2019/8549727
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