<?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>2026-10-19T00:27:41Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13583" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13583</identifier><datestamp>2026-10-18T21:13:28Z</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>Effects of adenosine triphosphate on methanol-induced experimental optic nerve damage in rats: biochemical and histopathological evaluation</dc:title><dc:creator>Icel, Erel</dc:creator><dc:creator>Suleyman, Halis</dc:creator><dc:creator>Yazici, Gulce Naz</dc:creator><dc:creator>Bakan, Nuri</dc:creator><dc:creator>Sunar, Mukadder</dc:creator><dc:subject>Adenosine triphosphate</dc:subject><dc:subject>methanol</dc:subject><dc:subject>optic nerve</dc:subject><dc:subject>oxidative stress</dc:subject><dc:subject>rats</dc:subject><dc:subject>Administration, Intravenous</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Glutathione</dc:subject><dc:subject>Male</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>Optic Nerve Injuries</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Solvents</dc:subject><dc:subject>distilled water</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>oxidizing agent</dc:subject><dc:subject>solvent</dc:subject><dc:subject>thiobarbituric acid</dc:subject><dc:subject>thiopental</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>antioxidant activity</dc:subject><dc:subject>Article</dc:subject><dc:subject>astrocyte</dc:subject><dc:subject>biochemical analysis</dc:subject><dc:subject>cell vacuole</dc:subject><dc:subject>clinical evaluation</dc:subject><dc:description>Purpose: Acute methanol exposure leads to systemic intoxication and toxic optic neuropathy. In this experimental study, we aimed to determine the protective effects of intravenous administration of ATP in methanol-induced optic neuropathy. Materials and methods: A total of 18 male albino Wistar rats weighing between 267 and 282 g were used for the experiment. The animals were divided into three groups as healthy control (HC), methanol (M), and methanol + ATP (M-ATP) groups. Distilled water was given to the healthy control group (n = 6) as the solvent, while 20% methanol was administered orally to the rats in M (n = 6) and M-ATP (n = 6) groups at a dose of 3 g/kg. Four hours after the administration of 20% methanol orally to the M-ATP group, ATP was injected intraperitoneally at a dose of 4 mg/kg. Eight hours after ATP injection, the animals were sacrificed by high-dose (50 mg/kg) thiopental anaesthesia and biochemical and histopathological examinations were performed on the removed optic nerve tissues. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS) and total anti-oxidant status (TAS) were analysed with biochemical tests. Results: MDA, TOS and OSI were significantly higher and tGSH and TAS levels were significantly lower in methanol administered group compared with the healthy controls or M-ATP group (p: 0.001). There was not any significant difference between healthy controls and M-ATP group regarding the oxidative stress parameters. There was a significant destruction and increase in thickness and astrocyte numbers and edema-vacuolization in methanol administered group compared with the healthy controls or M-ATP group (p: 0.001). Conclusion: Intravenous ATP administration had a significant positive effect on the oxidative stress parameters and optic nerve structure in methanol-intoxicated rats. Antioxidant therapies should be considered in future studies as a possible therapy for methanol-induced toxic optic neuropathy. © 2020 Informa UK Limited, trading as Taylor &amp; Francis Group.</dc:description><dc:publisher>Taylor and Francis Ltd.</dc:publisher><dc:date>2020</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/13583</dc:identifier><dc:identifier>https://doi.org/10.1080/15569527.2020.1778017</dc:identifier><dc:identifier>1556-9527</dc:identifier><dc:language>en</dc:language><dc:relation>Cutaneous and Ocular 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/13583</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>