<?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>2026-10-29T22:39:07Z</responseDate><request verb="GetRecord" identifier="oai:bayburt-rdlopen.rawdatalibrary.net:bayburt/10880" metadataPrefix="oai_dc">https://bayburt-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:bayburt-rdlopen.rawdatalibrary.net:bayburt/10880</identifier><datestamp>2026-10-29T19:41:13Z</datestamp><setSpec>openaire</setSpec><setSpec>com_bayburt_10000</setSpec><setSpec>col_bayburt_10001</setSpec><setSpec>com_bayburt_10010</setSpec><setSpec>col_bayburt_10222</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>A dual-acting aldose reductase inhibitor impedes oxidative and carbonyl stress in tissues of fructose- and streptozotocin-induced rats: comparison with antioxidant stobadine</dc:title><dc:creator>Kaya, Alican</dc:creator><dc:creator>Ceylan, Aslı F.</dc:creator><dc:creator>Kavutcu, Mustafa</dc:creator><dc:creator>Santamaria, Abel</dc:creator><dc:creator>Šoltésová Prnová, Marta</dc:creator><dc:creator>Stefek, Milan</dc:creator><dc:creator>Karasu, Çimen</dc:creator><dc:subject>aldose reductase</dc:subject><dc:subject>cemtirestat</dc:subject><dc:subject>Diabetes</dc:subject><dc:subject>epalrestat</dc:subject><dc:subject>fructose</dc:subject><dc:description>Inhibiting aldose reductase (ALR2, AR) as well as maintaining a concomitant antioxidant (AO) activity via dual-acting agents may be a rational approach to prevent cellular glucotoxicity and at least delay the progression of diabetes mellitus (DM). This study was aimed at evaluating the dual-acting AR inhibitor (ARI) cemtirestat (CMTI) on tissue oxidative stress (OS) and carbonyl stress (CS) biomarkers in rats exposed to fructose alone (F) or fructose plus streptozotocin (D; type-2 diabetic). D and F rats were either untreated or treated daily with low- or high-dose CMTI, ARI drug epalrestat (EPA) or antioxidant stobadine (STB) for 14 weeks. Malondialdehyde (MDA), glutathione S-transferase (GST), nitric oxide synthase (NOS), and catalase (CAT) were increased in the sciatic nerve of F and D. These increases were attenuated by low doses of CMTI and STB in D, but exacerbated by low-dose EPA and high-dose CMTI in F. STB and CMTI and to a lesser extent EPA improved MDA, protein-carbonyl, GST and CAT in the hearts and lungs of F and D. CMTI and STB were more effective than EPA in improving the increased MDA and protein-carbonyl levels in the kidneys of F and especially D. CMTI ameliorated renal GST inhibition in D. In the lungs, hearts, and kidneys of F and D, the GSH to GSSG ratio decreased and caspase-3 activity increased, but partially resolved with treatments. In conclusion, CMTI with ARI/AO activity may be advantageous in overcoming OS, CS, and their undesirable consequences, with low dose efficacy and limited toxicity, compared to ARI or antioxidant alone.</dc:description><dc:publisher>Taylor and Francis Ltd.</dc:publisher><dc:date>2024</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/bayburt/10880</dc:identifier><dc:identifier>https://doi.org/10.1080/01480545.2023.2262164</dc:identifier><dc:identifier>0148-0545</dc:identifier><dc:language>en</dc:language><dc:relation>Drug and Chemical Toxicology</dc:relation><dc:rights>info:eu-repo/semantics/closedAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://bayburt-rdlopen.rawdatalibrary.net/tr/items/bayburt/10880</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>