Effects of adenosine triphosphate on methanol-induced experimental optic nerve damage in rats: biochemical and histopathological evaluation

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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 & Francis Group.

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AlanDeğerDil
dc.contributor.authorIcel, Erel
dc.contributor.authorSuleyman, Halis
dc.contributor.authorYazici, Gulce Naz
dc.contributor.authorBakan, Nuri
dc.contributor.authorSunar, Mukadder
dc.date.accessioned2026-10-18T20:28:24.970839125Z
dc.date.available2026-10-18T20:28:24.970839125Z
dc.date.issued2020
dc.description.abstractPurpose: 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 & Francis Group.
dc.identifier.doi10.1080/15569527.2020.1778017
dc.identifier.eissn1556-9535
dc.identifier.endpage248
dc.identifier.issn1556-9527
dc.identifier.issue3
dc.identifier.pmid32543996
dc.identifier.scopus2-s2.0-85087441307
dc.identifier.startpage244
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13583
dc.identifier.volume39
dc.identifier.wosWOS:000548067300001
dc.language.isoen
dc.publisherTaylor and Francis Ltd.
dc.relation.ispartofCutaneous and Ocular Toxicology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAdenosine triphosphate
dc.subjectmethanol
dc.subjectoptic nerve
dc.subjectoxidative stress
dc.subjectrats
dc.subjectAdministration, Intravenous
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectGlutathione
dc.subjectMale
dc.subjectMalondialdehyde
dc.subjectOptic Nerve Injuries
dc.subjectRats, Wistar
dc.subjectSolvents
dc.subjectdistilled water
dc.subjectmalonaldehyde
dc.subjectoxidizing agent
dc.subjectsolvent
dc.subjectthiobarbituric acid
dc.subjectthiopental
dc.subjectantioxidant
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantioxidant activity
dc.subjectArticle
dc.subjectastrocyte
dc.subjectbiochemical analysis
dc.subjectcell vacuole
dc.subjectclinical evaluation
dc.titleEffects of adenosine triphosphate on methanol-induced experimental optic nerve damage in rats: biochemical and histopathological evaluation
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus15
rdl.citation.wos15
rdl.departmentFaculty of Medicine, Department of Ophthalmology, Erzincan Binali Yıldırım University, Erzincan, Turkey. | Faculty of Medicine, Department of Pharmacology, Erzincan Binali Yıldırım University, Erzincan, Turkey. | Faculty of Medicine, Department of Histology and Embryology, Erzincan Binali Yıldırım University, Erzincan, Turkey. | Faculty of Medicine, Department of Anatomy, Erzincan Binali Yıldırım University, Erzincan, Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)