<?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>2026-10-19T01:18:16Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/15022" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/15022</identifier><datestamp>2026-10-18T21:14:28Z</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>Benefical effects of lycopene against contrast medium-induced oxidative stress, inflammation, autophagy, and apoptosis in rat kidney</dc:title><dc:creator>Buyuklu, M.</dc:creator><dc:creator>Kandemir, F.M.</dc:creator><dc:creator>Ozkaraca, M.</dc:creator><dc:creator>Set, T.</dc:creator><dc:creator>Bakirci, E.M.</dc:creator><dc:creator>Topal, E.</dc:creator><dc:creator>Ileriturk, M.</dc:creator><dc:creator>Turkmen, K.</dc:creator><dc:subject>apoptosis</dc:subject><dc:subject>autophagy</dc:subject><dc:subject>Contrast nephropathy</dc:subject><dc:subject>inflammation</dc:subject><dc:subject>lycopene</dc:subject><dc:subject>oxidative stress</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Carotenoids</dc:subject><dc:subject>Contrast Media</dc:subject><dc:subject>Immunohistochemistry</dc:subject><dc:subject>Kidney</dc:subject><dc:subject>Male</dc:subject><dc:subject>Nephritis</dc:subject><dc:subject>Nitric Oxide Synthase Type II</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Rattus</dc:subject><dc:subject>caspase 3</dc:subject><dc:subject>catalase</dc:subject><dc:subject>creatinine</dc:subject><dc:subject>furosemide</dc:subject><dc:subject>glutathione</dc:subject><dc:subject>glutathione peroxidase</dc:subject><dc:subject>indometacin</dc:subject><dc:subject>inducible nitric oxide synthase</dc:subject><dc:subject>iomeprol</dc:subject><dc:subject>lc3 protein</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>peptides and proteins</dc:subject><dc:subject>reactive oxygen metabolite</dc:subject><dc:description>Currently, the number of imaging and interventional procedures that use contrast agents (CAs) is gradually increasing. Contrast-induced nephropathy (CIN) is the most important CA-related complication. Oxidative stress plays a significant role in its pathophysiology. Lycopene (LPN) is a natural substance with strong antioxidant capacity. The present study aimed to investigate the potential preventive effects of LPN against CIN. In total, 28 male Wistar albino rats were divided into 4 groups with 7 rats in each group; the groups include normal control group, LPN only group at a dose of 4 mg/kg/day for 10 days, CIN group by administering 10 mg/kg furosemide IM + 10 mg/kg indomethacin IP + 10 ml/kg iomeprol IV following 24-h dehydration, and CIN + LPN group. There were statistically significant increase in urea, creatinine, and malondialdehyde levels (p &lt; 0.001, for all) but a significant decrease in glutathione, superoxide dismutase, catalase, and glutathione peroxidase levels (p &lt; 0.001, for all) in the CIN group compared with the control group. On histological examination, a significant increase of infiltrated inflammatory cells and necrotic degenerative changes were observed in the CIN group and the immunohistochemical examination revealed a significant increase in inflammation (inducible nitric oxide synthase), autophagy (LC3/B), and apoptosis (cleaved caspase 3) in the CIN group compared with the control group (p &lt; 0.05, for all). Significant improvements in these unfavorable parameters were observed with CIN + LPN group compared with the CIN only group. In conclusion, the favorable effects of LPN as an anti-inflammatory, antiautophagic, and antiapoptotic agent in an experimental model of CIN have been demonstrated. © The Author(s) 2014.</dc:description><dc:publisher>SAGE Publications Ltd</dc:publisher><dc:date>2015</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/15022</dc:identifier><dc:identifier>https://doi.org/10.1177/0960327114542964</dc:identifier><dc:identifier>0960-3271</dc:identifier><dc:language>en</dc:language><dc:relation>Human and Experimental 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/15022</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>