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Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice
BACKGROUND: The goal of this study was to assess the effect of melatonin on blood redox systems in mice simultaneously exposed to ethanol and low-dose lipopolysaccharide (LPS). METHODS: Oxidative stress parameters were assessed in eight groups: untreated control, melatonin (10 mg kg(−1), 10 days), L...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8195796/ https://www.ncbi.nlm.nih.gov/pubmed/32968884 http://dx.doi.org/10.1007/s11325-020-02191-1 |
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author | Kurhaluk, Natalia Tkachenko, Halyna Lukash, Oleksandr Winklewski, Pawel J. Wszedybyl-Winklewska, Magdalena |
author_facet | Kurhaluk, Natalia Tkachenko, Halyna Lukash, Oleksandr Winklewski, Pawel J. Wszedybyl-Winklewska, Magdalena |
author_sort | Kurhaluk, Natalia |
collection | PubMed |
description | BACKGROUND: The goal of this study was to assess the effect of melatonin on blood redox systems in mice simultaneously exposed to ethanol and low-dose lipopolysaccharide (LPS). METHODS: Oxidative stress parameters were assessed in eight groups: untreated control, melatonin (10 mg kg(−1), 10 days), LPS (injected once intraperitoneally at a dose of 150 μg per mouse), LPS with previous melatonin treatment, acute ethanol-induced stress (AES, 0.75 g kg(−1) per day, 10 days), AES with previous melatonin treatment, LPS- and AES-induced toxicity, and melatonin treatment. RESULTS: Both ethanol and LPS induced oxidative stress. The combination of these two factors was even more toxic to the organism. Melatonin stabilized erythrocyte membranes and decreased the high level of free radical oxidation at the initial and final stages. Furthermore, melatonin limited protein damage through maintenance in the functional ability of the blood redox system to counteract pathological conditions. CONCLUSIONS: Melatonin limited the negative effects associated with alcohol consumption and low-intensity inflammation. |
format | Online Article Text |
id | pubmed-8195796 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-81957962021-06-28 Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice Kurhaluk, Natalia Tkachenko, Halyna Lukash, Oleksandr Winklewski, Pawel J. Wszedybyl-Winklewska, Magdalena Sleep Breath Psychiatrics • Original Article BACKGROUND: The goal of this study was to assess the effect of melatonin on blood redox systems in mice simultaneously exposed to ethanol and low-dose lipopolysaccharide (LPS). METHODS: Oxidative stress parameters were assessed in eight groups: untreated control, melatonin (10 mg kg(−1), 10 days), LPS (injected once intraperitoneally at a dose of 150 μg per mouse), LPS with previous melatonin treatment, acute ethanol-induced stress (AES, 0.75 g kg(−1) per day, 10 days), AES with previous melatonin treatment, LPS- and AES-induced toxicity, and melatonin treatment. RESULTS: Both ethanol and LPS induced oxidative stress. The combination of these two factors was even more toxic to the organism. Melatonin stabilized erythrocyte membranes and decreased the high level of free radical oxidation at the initial and final stages. Furthermore, melatonin limited protein damage through maintenance in the functional ability of the blood redox system to counteract pathological conditions. CONCLUSIONS: Melatonin limited the negative effects associated with alcohol consumption and low-intensity inflammation. Springer International Publishing 2020-09-23 2021 /pmc/articles/PMC8195796/ /pubmed/32968884 http://dx.doi.org/10.1007/s11325-020-02191-1 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Psychiatrics • Original Article Kurhaluk, Natalia Tkachenko, Halyna Lukash, Oleksandr Winklewski, Pawel J. Wszedybyl-Winklewska, Magdalena Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
title | Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
title_full | Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
title_fullStr | Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
title_full_unstemmed | Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
title_short | Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
title_sort | melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice |
topic | Psychiatrics • Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8195796/ https://www.ncbi.nlm.nih.gov/pubmed/32968884 http://dx.doi.org/10.1007/s11325-020-02191-1 |
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