Alterations of Bio-elements, Oxidative, and Inflammatory Status in the Zinc Deficiency Model in Rats

Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N -methyl- d -aspartate receptor (NMDAR). Because metal ions, oxidative stress, and inflammation are involved in depression/NMDAR function, in the present study, bio-element...

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Vydané v:	Neurotoxicity research Ročník 29; číslo 1; s. 143 - 154
Hlavní autori:	Doboszewska, Urszula, Szewczyk, Bernadeta, Sowa-Kućma, Magdalena, Noworyta-Sokołowska, Karolina, Misztak, Paulina, Gołębiowska, Joanna, Młyniec, Katarzyna, Ostachowicz, Beata, Krośniak, Mirosław, Wojtanowska-Krośniak, Agnieszka, Gołembiowska, Krystyna, Lankosz, Marek, Piekoszewski, Wojciech, Nowak, Gabriel
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	New York Springer US 01.01.2016
Predmet:	Animals Biomedical and Life Sciences Biomedicine Body Weight Cell Biology Copper - metabolism Corticosterone - metabolism Diet - adverse effects Dose-Response Relationship, Drug Hippocampus - metabolism Interleukin-1alpha - blood Interleukin-1beta - blood Iron - metabolism Male Neurobiology Neurochemistry Neurology Neurosciences Original Original Article Oxidative Stress - drug effects Pharmacology/Toxicology Potassium Chloride - pharmacology Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Protein Carbonylation - drug effects Rats Rats, Sprague-Dawley Thiobarbituric Acid Reactive Substances - metabolism Time Factors Zinc - administration & dosage Zinc - blood Zinc - deficiency Iron Oxidation Inflammation Zinc deficiency Glutamate Zinc
ISSN:	1029-8428, 1476-3524
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Abstract	Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N -methyl- d -aspartate receptor (NMDAR). Because metal ions, oxidative stress, and inflammation are involved in depression/NMDAR function, in the present study, bio-elements (zinc, copper, iron, magnesium, and calcium), oxidative (thiobarbituric acid-reactive substances; protein carbonyl content), and inflammatory (IL-1α, IL-1β) factors were measured in serum, hippocampus (Hp), and prefrontal cortex (PFC) of male Sprague–Dawley rats subjected to a zinc-adequate (ZnA) (50 mg Zn/kg) or a zinc-deficient (ZnD) (3 mg Zn/kg) diet for 4 or 6 weeks. Both periods of dietary zinc restriction reduced serum zinc and increased serum iron levels. At 4 weeks, lowered zinc level in the PFC and Hp as well as lowered iron level in the PFC of the ZnD rats was observed. At 6 weeks, however, iron level was increased in the PFC of these rats. Although at 6 weeks zinc level in the PFC did not differ between the ZnA and ZnD rats, extracellular zinc concentration after 100 mM KCl stimulation was reduced in the PFC of the ZnD rats and was accompanied by increased extracellular iron and glutamate levels (as measured by the in vivo microdialysis). The examined oxidative and inflammatory parameters were generally enhanced in the tissue of the ZnD animals. The obtained data suggest dynamic redistribution of bio-elements and enhancement of oxidative/inflammatory parameters after dietary zinc restriction, which may have a link with depression-like behavior/NMDAR function/neurodegeneration.
AbstractList	Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N -methyl- d -aspartate receptor (NMDAR). Because metal ions, oxidative stress, and inflammation are involved in depression/NMDAR function, in the present study, bio-elements (zinc, copper, iron, magnesium, and calcium), oxidative (thiobarbituric acid-reactive substances; protein carbonyl content), and inflammatory (IL-1α, IL-1β) factors were measured in serum, hippocampus (Hp), and prefrontal cortex (PFC) of male Sprague–Dawley rats subjected to a zinc-adequate (ZnA) (50 mg Zn/kg) or a zinc-deficient (ZnD) (3 mg Zn/kg) diet for 4 or 6 weeks. Both periods of dietary zinc restriction reduced serum zinc and increased serum iron levels. At 4 weeks, lowered zinc level in the PFC and Hp as well as lowered iron level in the PFC of the ZnD rats was observed. At 6 weeks, however, iron level was increased in the PFC of these rats. Although at 6 weeks zinc level in the PFC did not differ between the ZnA and ZnD rats, extracellular zinc concentration after 100 mM KCl stimulation was reduced in the PFC of the ZnD rats and was accompanied by increased extracellular iron and glutamate levels (as measured by the in vivo microdialysis). The examined oxidative and inflammatory parameters were generally enhanced in the tissue of the ZnD animals. The obtained data suggest dynamic redistribution of bio-elements and enhancement of oxidative/inflammatory parameters after dietary zinc restriction, which may have a link with depression-like behavior/NMDAR function/neurodegeneration. Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N-methyl-d-aspartate receptor (NMDAR). Because metal ions, oxidative stress, and inflammation are involved in depression/NMDAR function, in the present study, bio-elements (zinc, copper, iron, magnesium, and calcium), oxidative (thiobarbituric acid-reactive substances; protein carbonyl content), and inflammatory (IL-1α, IL-1β) factors were measured in serum, hippocampus (Hp), and prefrontal cortex (PFC) of male Sprague–Dawley rats subjected to a zinc-adequate (ZnA) (50 mg Zn/kg) or a zinc-deficient (ZnD) (3 mg Zn/kg) diet for 4 or 6 weeks. Both periods of dietary zinc restriction reduced serum zinc and increased serum iron levels. At 4 weeks, lowered zinc level in the PFC and Hp as well as lowered iron level in the PFC of the ZnD rats was observed. At 6 weeks, however, iron level was increased in the PFC of these rats. Although at 6 weeks zinc level in the PFC did not differ between the ZnA and ZnD rats, extracellular zinc concentration after 100 mM KCl stimulation was reduced in the PFC of the ZnD rats and was accompanied by increased extracellular iron and glutamate levels (as measured by the in vivo microdialysis). The examined oxidative and inflammatory parameters were generally enhanced in the tissue of the ZnD animals. The obtained data suggest dynamic redistribution of bio-elements and enhancement of oxidative/inflammatory parameters after dietary zinc restriction, which may have a link with depression-like behavior/NMDAR function/neurodegeneration. Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N-methyl-D-aspartate receptor (NMDAR). Because metal ions, oxidative stress, and inflammation are involved in depression/NMDAR function, in the present study, bio-elements (zinc, copper, iron, magnesium, and calcium), oxidative (thiobarbituric acid-reactive substances; protein carbonyl content), and inflammatory (IL-1α, IL-1β) factors were measured in serum, hippocampus (Hp), and prefrontal cortex (PFC) of male Sprague-Dawley rats subjected to a zinc-adequate (ZnA) (50 mg Zn/kg) or a zinc-deficient (ZnD) (3 mg Zn/kg) diet for 4 or 6 weeks. Both periods of dietary zinc restriction reduced serum zinc and increased serum iron levels. At 4 weeks, lowered zinc level in the PFC and Hp as well as lowered iron level in the PFC of the ZnD rats was observed. At 6 weeks, however, iron level was increased in the PFC of these rats. Although at 6 weeks zinc level in the PFC did not differ between the ZnA and ZnD rats, extracellular zinc concentration after 100 mM KCl stimulation was reduced in the PFC of the ZnD rats and was accompanied by increased extracellular iron and glutamate levels (as measured by the in vivo microdialysis). The examined oxidative and inflammatory parameters were generally enhanced in the tissue of the ZnD animals. The obtained data suggest dynamic redistribution of bio-elements and enhancement of oxidative/inflammatory parameters after dietary zinc restriction, which may have a link with depression-like behavior/NMDAR function/neurodegeneration.
Author	Noworyta-Sokołowska, Karolina Wojtanowska-Krośniak, Agnieszka Młyniec, Katarzyna Krośniak, Mirosław Piekoszewski, Wojciech Nowak, Gabriel Lankosz, Marek Misztak, Paulina Szewczyk, Bernadeta Sowa-Kućma, Magdalena Ostachowicz, Beata Gołębiowska, Joanna Doboszewska, Urszula Gołembiowska, Krystyna
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Keywords	Iron Oxidation Inflammation Zinc deficiency Glutamate Zinc
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Snippet	Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N -methyl- d -aspartate receptor... Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N-methyl-D-aspartate receptor... Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N-methyl-d-aspartate receptor...
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SubjectTerms	Animals Biomedical and Life Sciences Biomedicine Body Weight Cell Biology Copper - metabolism Corticosterone - metabolism Diet - adverse effects Dose-Response Relationship, Drug Hippocampus - metabolism Interleukin-1alpha - blood Interleukin-1beta - blood Iron - metabolism Male Neurobiology Neurochemistry Neurology Neurosciences Original Original Article Oxidative Stress - drug effects Pharmacology/Toxicology Potassium Chloride - pharmacology Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Protein Carbonylation - drug effects Rats Rats, Sprague-Dawley Thiobarbituric Acid Reactive Substances - metabolism Time Factors Zinc - administration & dosage Zinc - blood Zinc - deficiency
Title	Alterations of Bio-elements, Oxidative, and Inflammatory Status in the Zinc Deficiency Model in Rats
URI	https://link.springer.com/article/10.1007/s12640-015-9571-7 https://www.ncbi.nlm.nih.gov/pubmed/26581375 https://www.proquest.com/docview/1754523336 https://pubmed.ncbi.nlm.nih.gov/PMC4701762
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