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Prevention of selenite‐induced cataractogenesis by sildenafil in rats
Author(s) -
Atalay H.T.,
Üçgül A.Y.,
Özel Türkçü Ü.,
Özmen M.C.,
Yılmaz N.S.,
Bilgihan A.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.03583
Subject(s) - sildenafil , selenium , medicine , nitrite , nitric oxide , endocrinology , chemistry , organic chemistry , nitrate
Purpose To evaluate the effect of sildenafil on selenite‐induced cataract formation in a rat model. Methods Twenty‐six Wistar rat pups were divided into four groups. Seven pups received only selenite on postpartum day 10 (group 1), 7 pups received selenite and additional high dose sildenafil on postpartum day 10 (group 2), 6 pups received selenite and additional low dose sildenafil on postpartum day 10 (group 3), and 6 pups received only saline (group 4, control). All pups were examined for the presence of cataract under the microscope, starting from the day their eyes opened. Nitrite oxide metabolites, advanced oxidation protein products and total sulfhydryl levels were evaluated in both serum and lenticular samples. Results In group 3, the extent of lens opacification was significantly less than that of selenite‐injected untreated rats (group 1) (p < 0.05). None of the rats in group 4 developed any lens opacity. In lenticular samples, nitrite oxide metabolites level was statistically lower in group 3 compared to group 1 (p < 0.05). In serum, advanced oxidation protein products and total sulfhydryl levels was statistically lower in group 3 compared to group 1 (p < 0.05). Conclusions Low dose sildenafil appears to inhibit selenite‐induced cataractogenesis in the rat model, and this seems to be caused by the prevention of oxidative damage.