<?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>2026-10-19T00:34:12Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/20080" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/20080</identifier><datestamp>2026-10-18T21:12:00Z</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 Ethanol-Induced OxidativeBbrain Damage in Rats</dc:title><dc:creator>BİLGİN, ASLI ÖZBEK</dc:creator><dc:creator>SÜLEYMAN, BAHADIR</dc:creator><dc:creator>Mammadov, Renad</dc:creator><dc:subject>Tıbbi Araştırmalar Deneysel</dc:subject><dc:subject>Klinik Nöroloji</dc:subject><dc:subject>Nörolojik Bilimler</dc:subject><dc:subject>Fizyoloji</dc:subject><dc:subject>Biyokimya ve Moleküler Biyoloji</dc:subject><dc:description>Studies have shown that alcohol exerts the most severe toxic effect on central nervous system by increasing free oxygen radical production and suppressing endogenous antioxidant production. We aim to biochemically investigate the effect of taxifolin on ethanol-induced oxidative brain damage in rats. ( Sakarya Med J, 2018, 8(3):638-643 ). Materials and Methods Experimental animals were divided into healthy (SG), ethanol-receiving control (EtOH) and taxifolin+ethanol receiving (TEtOH) groups. At the end of the administration of ethanol and taxifolin, the animals were sacrifi ced by high dose anesthesia and brain tissues were removed. Malondialdehyde (MDA), lipid peroxidation product, and total glutathione (tGSH), endogenous antioxidant, levels in brain tissues were measured. Results MDA levels were signifi cantly higher in the rats in the EtOH group than in those in the TEtOH group (p&lt;0.001). In contrast, tGSH levels were signifi cantly lower in the rats in the EtOH group than in those in the TEtOH group (p&lt;0.001). Conclusion Our results suggest that taxifolin protects brain tissue from ethanol-induced oxidative damage.</dc:description><dc:date>2018</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/20080</dc:identifier><dc:language>tr</dc:language><dc:relation>Sakarya Tıp Dergisi</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/20080</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>