<?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>2026-10-19T03:29:46Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/17010" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/17010</identifier><datestamp>2026-10-18T21:13:25Z</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>The role of protein oxidation in the development of diabetic microvascular complications</dc:title><dc:creator>Mertoglu, Cuma</dc:creator><dc:creator>Siranli, Gulsah</dc:creator><dc:creator>Coban, T. Abdulkadir</dc:creator><dc:creator>Karakurt, Yucel</dc:creator><dc:creator>Ersoy, Alevtina</dc:creator><dc:creator>Ozcicek, Adalet</dc:creator><dc:creator>Arslan, Yusuf</dc:creator><dc:creator>Gok, Gamze</dc:creator><dc:creator>Erel, Ozcan</dc:creator><dc:subject>Diabetes mellitus</dc:subject><dc:subject>microvascular complications</dc:subject><dc:subject>neuropathy</dc:subject><dc:subject>retinopathy</dc:subject><dc:subject>thiol-disulfide</dc:subject><dc:subject>AUTOMATED-ASSAY</dc:subject><dc:subject>ALBUMIN</dc:subject><dc:subject>HOMEOSTASIS</dc:subject><dc:subject>MECHANISMS</dc:subject><dc:subject>DISEASE</dc:subject><dc:subject>Medicine, General &amp; Internal</dc:subject><dc:subject>General &amp; Internal Medicine</dc:subject><dc:description>OBJECTIVE: The role of protein oxidation in the development of diabetic microvascular complications was investigated. METHODS: In total, 266 participants were split into five groups: Group 1; diabetes mellitus for at least 10 years without any complications, Group 2; diabetic nephropathy, Group 3; diabetic neuropathy, Group 4; diabetic retinopathy, and Group 5; control group. Thiol, disulfide, ferroxidase, and ischemia-modified albumin (IMA) levels were analyzed in the serum. RESULTS: Native thiol, total thiol, and native thiol/total thiol were lower in Group 4 than Groups 1, 3, and 5 (p&lt;0.001). However, disulfide/native thiol and disulfide/total thiol were higher in Group 4 than all other groups (p&lt;0.001). IMA was higher in Groups 3 and 4 than all other groups (p&lt;0.001). Ferroxidase was lower in Groups 3 and 4 than Group 2 (p&lt;0.001). CONCLUSION: Thiol-disulfide homeostasis impairment in favor of disulfide may have a function in the progress of diabetic retinopathy. Furthermore, the disruptions of IMA and ferroxidase levels involve in the development of diabetic retinopathy and neuropathy.</dc:description><dc:publisher>KARE PUBL</dc:publisher><dc:date>2021</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/17010</dc:identifier><dc:identifier>https://doi.org/10.14744/nci.2021.33341</dc:identifier><dc:identifier>2148-4902</dc:identifier><dc:language>en</dc:language><dc:relation>NORTHERN CLINICS OF ISTANBUL</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/17010</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>