<?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>2026-10-19T01:08:46Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13731" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13731</identifier><datestamp>2026-10-18T21:13:30Z</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 taxifolin on methanol-induced oxidative and inflammatory optic nerve damage in rats</dc:title><dc:creator>Ahiskali, Ibrahim</dc:creator><dc:creator>Pinar, Can Lokman</dc:creator><dc:creator>Kiki, Murat</dc:creator><dc:creator>Cankaya, Murat</dc:creator><dc:creator>Kunak, Celaleddin Semih</dc:creator><dc:creator>Altuner, Durdu</dc:creator><dc:subject>damage</dc:subject><dc:subject>methanol</dc:subject><dc:subject>optic nerve</dc:subject><dc:subject>Taxifolin</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Anti-Inflammatory Agents</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Glutathione</dc:subject><dc:subject>Male</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>NF-kappa B</dc:subject><dc:subject>Optic Nerve Injuries</dc:subject><dc:subject>Oxidative Stress</dc:subject><dc:subject>Quercetin</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Solvents</dc:subject><dc:subject>Tumor Necrosis Factor-alpha</dc:subject><dc:subject>immunoglobulin enhancer binding protein</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>methotrexate</dc:subject><dc:subject>thiopental</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>antiinflammatory agent</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>solvent</dc:subject><dc:subject>anesthesia</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>antiinflammatory activity</dc:subject><dc:description>Purpose: Oxidative stress and inflammation have been demonstrated in the pathogenesis of methanol toxicity. Taxifolin has antioxidant and anti-inflammatory properties. In this study, we examined the protective effect of taxifolin against methanol-induced optic nerve toxicity. Materials and methods: Animals were divided into four groups (n = 6): healthy control group (HG), methotrexate (MTX) treated group, methotrexate + methanol treated group (MTX + M), and methotrexate + methanol + taxifolin treated group (MTX + M+T). MTX was administered to all groups except HG group 3 mg/kg via oral gavage for 7 d. After that 20% methanol was orally administered to the MTX + M and MTX + M+T group at a dose of 3 g/kg. After 4 h, taxifolin was orally administered to MTX + M+T group 50 mg/kg. Animals were sacrificed by high-dose thiopental anaesthesia, 8 h after taxifolin administration and biochemical studies were performed. Results: Malondialdehyde (MDA), total oxidant system, nuclear factor kappa B (NF-κB), and tumour necrosis factor-alpha levels were significantly higher in the optic nerve of MTX and MTX + M groups compared to HG group. Otherwise, total glutathione (tGSH) and total antioxidant system levels decreased in MTX and MTX + M groups according to the HG group. MDA, total oxidant system, NF-κB, and tumour necrosis factor-alpha levels were decreased in the MTX + M+T group and tGSH, and total antioxidant system levels increased in the MTX + M+T group according to the MTX + M group. Conclusions: These results indicate that taxifolin prevents oxidative and inflammatory optic nerve damage due to methanol exposure. © 2019, © 2019 Informa UK Limited, trading as Taylor &amp; Francis Group.</dc:description><dc:publisher>Taylor and Francis Ltd</dc:publisher><dc:date>2019</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/13731</dc:identifier><dc:identifier>https://doi.org/10.1080/15569527.2019.1637348</dc:identifier><dc:identifier>1556-9527</dc:identifier><dc:language>en</dc:language><dc:relation>Cutaneous and Ocular Toxicology</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/13731</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>