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Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life

The aim of the present study was to assess the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and GBR 12909, a dopamine reuptake inhibitor, administered alone or in combination to Sprague-Dawley rats during early postnatal development (p5–p16), on the level...

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Autores principales: Górny, Magdalena, Bilska-Wilkosz, Anna, Iciek, Małgorzata, Hereta, Marta, Kamińska, Kinga, Kamińska, Adrianna, Chwatko, Grażyna, Rogóż, Zofia, Lorenc-Koci, Elżbieta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346228/
https://www.ncbi.nlm.nih.gov/pubmed/32575563
http://dx.doi.org/10.3390/antiox9060538
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author Górny, Magdalena
Bilska-Wilkosz, Anna
Iciek, Małgorzata
Hereta, Marta
Kamińska, Kinga
Kamińska, Adrianna
Chwatko, Grażyna
Rogóż, Zofia
Lorenc-Koci, Elżbieta
author_facet Górny, Magdalena
Bilska-Wilkosz, Anna
Iciek, Małgorzata
Hereta, Marta
Kamińska, Kinga
Kamińska, Adrianna
Chwatko, Grażyna
Rogóż, Zofia
Lorenc-Koci, Elżbieta
author_sort Górny, Magdalena
collection PubMed
description The aim of the present study was to assess the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and GBR 12909, a dopamine reuptake inhibitor, administered alone or in combination to Sprague-Dawley rats during early postnatal development (p5–p16), on the levels of reactive oxygen species (ROS), lipid peroxidation (LP) and the activities of antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione disulfide reductase (GR) in peripheral tissues (liver, kidney) and selected brain structures (prefrontal cortex, PFC; hippocampus, HIP; and striatum, STR) of 16-day-old rats. The studied parameters were analyzed with reference to the content of GSH and sulfur amino acids, methionine (Met) and cysteine (Cys) described in our previous study. This analysis showed that treatment with a BSO + GBR 12909 combination caused significant decreases in the lipid peroxidation levels in the PFC and HIP, in spite of there being no changes in ROS. The reduction of lipid peroxidation indicates a weakening of the oxidative power of the cells, and a shift in balance in favor of reducing processes. Such changes in cellular redox signaling in the PFC and HIP during early postnatal development may result in functional changes in adulthood.
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spelling pubmed-73462282020-07-20 Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life Górny, Magdalena Bilska-Wilkosz, Anna Iciek, Małgorzata Hereta, Marta Kamińska, Kinga Kamińska, Adrianna Chwatko, Grażyna Rogóż, Zofia Lorenc-Koci, Elżbieta Antioxidants (Basel) Article The aim of the present study was to assess the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and GBR 12909, a dopamine reuptake inhibitor, administered alone or in combination to Sprague-Dawley rats during early postnatal development (p5–p16), on the levels of reactive oxygen species (ROS), lipid peroxidation (LP) and the activities of antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione disulfide reductase (GR) in peripheral tissues (liver, kidney) and selected brain structures (prefrontal cortex, PFC; hippocampus, HIP; and striatum, STR) of 16-day-old rats. The studied parameters were analyzed with reference to the content of GSH and sulfur amino acids, methionine (Met) and cysteine (Cys) described in our previous study. This analysis showed that treatment with a BSO + GBR 12909 combination caused significant decreases in the lipid peroxidation levels in the PFC and HIP, in spite of there being no changes in ROS. The reduction of lipid peroxidation indicates a weakening of the oxidative power of the cells, and a shift in balance in favor of reducing processes. Such changes in cellular redox signaling in the PFC and HIP during early postnatal development may result in functional changes in adulthood. MDPI 2020-06-19 /pmc/articles/PMC7346228/ /pubmed/32575563 http://dx.doi.org/10.3390/antiox9060538 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Górny, Magdalena
Bilska-Wilkosz, Anna
Iciek, Małgorzata
Hereta, Marta
Kamińska, Kinga
Kamińska, Adrianna
Chwatko, Grażyna
Rogóż, Zofia
Lorenc-Koci, Elżbieta
Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life
title Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life
title_full Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life
title_fullStr Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life
title_full_unstemmed Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life
title_short Alterations in the Antioxidant Enzyme Activities in the Neurodevelopmental Rat Model of Schizophrenia Induced by Glutathione Deficiency during Early Postnatal Life
title_sort alterations in the antioxidant enzyme activities in the neurodevelopmental rat model of schizophrenia induced by glutathione deficiency during early postnatal life
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346228/
https://www.ncbi.nlm.nih.gov/pubmed/32575563
http://dx.doi.org/10.3390/antiox9060538
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