<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-19T01:56:20Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13704" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13704</identifier><datestamp>2026-10-18T21:14:19Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_ebyu_10000</setSpec><setSpec>col_ebyu_10001</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>Effect of lutein on methotrexate-induced oxidative lung damage in rats: A biochemical and histopathological assessment</dc:title><dc:creator>Mammadov, Renad</dc:creator><dc:creator>Suleyman, Bahadir</dc:creator><dc:creator>Akturan, Selcuk</dc:creator><dc:creator>Cimen, Ferda Keskin</dc:creator><dc:creator>Kurt, Nezahat</dc:creator><dc:creator>Suleyman, Zeynep</dc:creator><dc:creator>Malkoc, İsmail</dc:creator><dc:subject>Lung</dc:subject><dc:subject>Lutein</dc:subject><dc:subject>Methotrexate</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Disease Models, Animal</dc:subject><dc:subject>Glutathione</dc:subject><dc:subject>Interleukin-1beta</dc:subject><dc:subject>Lung Diseases</dc:subject><dc:subject>Male</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>Oxidative Stress</dc:subject><dc:subject>Peroxidase</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Tumor Necrosis Factor-alpha</dc:subject><dc:subject>interleukin 1beta</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>myeloperoxidase</dc:subject><dc:subject>sodium chloride</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>xanthophyll</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>IL1B protein, rat</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>Article</dc:subject><dc:subject>biochemistry</dc:subject><dc:subject>controlled study</dc:subject><dc:subject>drug effect</dc:subject><dc: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 &lt; 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. © 2019 The Korean Association of Internal Medicine.</dc:description><dc:publisher>Korean Association of Internal Medicine</dc:publisher><dc:date>2019</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/13704</dc:identifier><dc:identifier>https://doi.org/10.3904/kjim.2018.145</dc:identifier><dc:identifier>1226-3303</dc:identifier><dc:language>en</dc:language><dc:relation>Korean Journal of Internal Medicine</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/13704</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>