2026-10-19T00:01:59Zhttps://ebyu-rdlopen.rawdatalibrary.net/oai/requestoai:ebyu-rdlopen.rawdatalibrary.net:ebyu/107442026-10-18T21:13:09Zopenairedrivercom_ebyu_10000col_ebyu_10001Pathophysiology of sildenafil-induced ocular toxicity in rats and treatmentCicek, IbrahimCaliskan, BusraYavuzer, BulentAltuner, DurduTastan, Tugba BalCoban, Taha AbdulkadirKaratas, EzgiSuleyman, Halisadenosine triphosphateocular toxicityoxidative stressratsretinasildenafilcatalasedegraglutathionemalonaldehydepental sodyumsuperoxide dismutasethiopentalzdorovye naroduacclimatizationanimal experimentanimal modelanimal tissueantioxidant parametersArticlecell infiltrationcontrolled studyenzyme linked immunosorbent assayeye toxicityhistopathologymalenonhumanparameterspathophysiologypolymorphonuclear cell infiltrationRESULTS: Sildenafil increased oxidant (malondialdehyde) levels and decreased antioxidant levels (total glutathione, superoxide dismutase, catalase) in rat ocular tissues and caused severe oxidative stress. In addition, sildenafil has been shown histopathologically to cause oxidative damage in retinal layers. ATP treatment suppressed oxidative stress and attenuated histopathological damage in the retinal layers. CONCLUSION: ATP protects retinal tissue against sildenafil-induced ocular oxidative damage in rats and may contribute to the development of novel approaches to prevent or treat this damage. © (2026), (International Journal of Ophthalmology (c/o Editorial Office)). All Rigths Reserved.International Journal of Ophthalmology (c/o Editorial Office)2026Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/10744https://doi.org/10.18240/ijo.2026.01.032222-3959enInternational Journal of Ophthalmologyinfo:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/10744