<?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>2026-10-19T00:02:39Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/11447" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/11447</identifier><datestamp>2026-10-18T21:13:13Z</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>Potential effects of adenosine triphosphate and melatonin on oxidative and inflammatory optic nerve damage in rats caused by 5-fluorouracil</dc:title><dc:creator>Somuncu, Ahmet Mehmet</dc:creator><dc:creator>Somuncu, Busra Parlak</dc:creator><dc:creator>Ozbay, Ahmet Duhan</dc:creator><dc:creator>Cicek, Ibrahim</dc:creator><dc:creator>Suleyman, Bahadir</dc:creator><dc:creator>Mammadov, Renad</dc:creator><dc:creator>Bulut, Seval</dc:creator><dc:creator>Tastan, Tugba Bal</dc:creator><dc:creator>Coban, Taha Abdulkadir</dc:creator><dc:creator>Suleyman, Halis</dc:creator><dc:creator>Aydin, Aliyev</dc:creator><dc:subject>5-fluorouracil</dc:subject><dc:subject>adenosine triphosphate</dc:subject><dc:subject>anti-inflammatory</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>melatonin</dc:subject><dc:subject>optic nerve damage</dc:subject><dc:subject>fluorouracil</dc:subject><dc:subject>glutathione</dc:subject><dc:subject>glutathione peroxidase</dc:subject><dc:subject>glutathione reductase</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>superoxide dismutase</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>antiinflammatory activity</dc:subject><dc:subject>antioxidant activity</dc:subject><dc:subject>Article</dc:subject><dc:subject>astrocyte</dc:subject><dc:subject>controlled study</dc:subject><dc:subject>cytokine production</dc:subject><dc:subject>enzyme linked immunosorbent assay</dc:subject><dc:subject>histopathology</dc:subject><dc:subject>inflammation</dc:subject><dc:subject>lipid peroxidation</dc:subject><dc:subject>male</dc:subject><dc:subject>mouse</dc:subject><dc:subject>nonhuman</dc:subject><dc:subject>optic nerve</dc:subject><dc:subject>optic nerve lesion</dc:subject><dc:description>• AIM: To investigate the effects of adenosine triphosphate (ATP) and melatonin, which have antioxidant and anti-inflammatory activities, on potential 5-fluorouracil (5-FU)-induced optic nerve damage in rats. • METHODS: Twenty-four rats were categorized into four groups of six rats: healthy (HG), 5-FU (FUG), ATP+5-FU (AFU), and melatonin+5-FU (MFU). ATP (4 mg/kg) and melatonin (10 mg/kg) were administered intraperitoneally and orally, respectively. One hour after ATP and melatonin administration, rats in the AFU, MFU, and FUG were intraperitoneally injected with 5-FU (100 mg/kg). ATP and melatonin were administered once daily for 10d. 5-FU was administered at a single dose on days 1, 3, and 5 of the experiment. After 10d, the rats were euthanized and optic nerve tissues were extracted. Optic nerve tissues were biochemically and histopathologically examined. • RESULTS: ATP and melatonin treatments inhibited the increase in malondialdehyde (MDA) and interleukin-6 (IL-6) levels, which were elevated in the FUG. The treatments also prevented the decrease in total glutathione (tGSH) levels and the superoxide dismutase (SOD) and catalase (CAT) activities (P&lt;0.001). This inhibition was higher in the ATP group than in the melatonin group (P&lt;0.001). ATP prevented histopathological damage better than melatonin (P&lt;0.05). • CONCLUSION: ATP and melatonin have the potential to be used in alleviating 5-FU-induced optic nerve damage. In addition, ATP treatment shows better protective effects than melatonin. © 2025 International Journal of Ophthalmology (c/o Editorial Office). All rights reserved.</dc:description><dc:publisher>International Journal of Ophthalmology (c/o Editorial Office)</dc:publisher><dc:date>2025</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/11447</dc:identifier><dc:identifier>https://doi.org/10.18240/ijo.2025.02.04</dc:identifier><dc:identifier>2222-3959</dc:identifier><dc:language>en</dc:language><dc:relation>International Journal of Ophthalmology</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/11447</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>