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Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment
BACKGROUND/AIMS: This study aimed to investigate the effect of lutein on methotrexate (MTX)-induced pulmonary toxicity in rats biochemically and histopathologically. METHODS: The rats in the MTX + lutein (MTXL, n = 6) group were given 1 mg/kg of lutein orally. A 0.9% NaCl solution was administered o...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Association of Internal Medicine
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823580/ https://www.ncbi.nlm.nih.gov/pubmed/31495083 http://dx.doi.org/10.3904/kjim.2018.145 |
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author | Mammadov, Renad Suleyman, Bahadir Akturan, Selcuk Cimen, Ferda Keskin Kurt, Nezahat Suleyman, Zeynep Malkoc, İsmail |
author_facet | Mammadov, Renad Suleyman, Bahadir Akturan, Selcuk Cimen, Ferda Keskin Kurt, Nezahat Suleyman, Zeynep Malkoc, İsmail |
author_sort | Mammadov, Renad |
collection | PubMed |
description | BACKGROUND/AIMS: This study aimed to investigate the effect of lutein on methotrexate (MTX)-induced pulmonary toxicity in rats biochemically and histopathologically. METHODS: The rats in the MTX + lutein (MTXL, n = 6) group were given 1 mg/kg of lutein orally. A 0.9% NaCl solution was administered orally to the MTX (n = 6) group and the healthy group (HG, n = 6). One hour later, a single 20 mg/kg dose of MTX was injected intraperitoneally in the MTXL and MTX. Lutein or 0.9% NaCl solution was administered once a day for 5 days. At the end of this period, malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) were measured in the lung tissues from the animals euthanized with 50 mg/kg thiopental sodium anesthesia. Subsequently, histopathological examinations were performed. RESULTS: The levels of MDA, MPO, IL-1β, and TNF-α in the lung tissue of the MTX were significantly higher than those of the MTXL and HG groups (p < 0.0001), and the amount of tGSH was lower. The histopathological findings in the MTX group, in which the oxidants and cytokines were higher, were more severe. CONCLUSIONS: Lutein prevented the MTX-induced oxidative lung damage biochemically and histopathologically. This result indicates that lutein may be useful in the treatment of MTX-induced lung damage. |
format | Online Article Text |
id | pubmed-6823580 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The Korean Association of Internal Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-68235802019-11-12 Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment Mammadov, Renad Suleyman, Bahadir Akturan, Selcuk Cimen, Ferda Keskin Kurt, Nezahat Suleyman, Zeynep Malkoc, İsmail Korean J Intern Med Original Article BACKGROUND/AIMS: This study aimed to investigate the effect of lutein on methotrexate (MTX)-induced pulmonary toxicity in rats biochemically and histopathologically. METHODS: The rats in the MTX + lutein (MTXL, n = 6) group were given 1 mg/kg of lutein orally. A 0.9% NaCl solution was administered orally to the MTX (n = 6) group and the healthy group (HG, n = 6). One hour later, a single 20 mg/kg dose of MTX was injected intraperitoneally in the MTXL and MTX. Lutein or 0.9% NaCl solution was administered once a day for 5 days. At the end of this period, malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) were measured in the lung tissues from the animals euthanized with 50 mg/kg thiopental sodium anesthesia. Subsequently, histopathological examinations were performed. RESULTS: The levels of MDA, MPO, IL-1β, and TNF-α in the lung tissue of the MTX were significantly higher than those of the MTXL and HG groups (p < 0.0001), and the amount of tGSH was lower. The histopathological findings in the MTX group, in which the oxidants and cytokines were higher, were more severe. CONCLUSIONS: Lutein prevented the MTX-induced oxidative lung damage biochemically and histopathologically. This result indicates that lutein may be useful in the treatment of MTX-induced lung damage. The Korean Association of Internal Medicine 2019-11 2019-09-10 /pmc/articles/PMC6823580/ /pubmed/31495083 http://dx.doi.org/10.3904/kjim.2018.145 Text en Copyright © 2019 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Mammadov, Renad Suleyman, Bahadir Akturan, Selcuk Cimen, Ferda Keskin Kurt, Nezahat Suleyman, Zeynep Malkoc, İsmail Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
title | Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
title_full | Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
title_fullStr | Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
title_full_unstemmed | Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
title_short | Effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
title_sort | effect of lutein on methotrexate-induced oxidative lung damage in rats: a biochemical and histopathological assessment |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823580/ https://www.ncbi.nlm.nih.gov/pubmed/31495083 http://dx.doi.org/10.3904/kjim.2018.145 |
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