Fluoksetin hidroklorürün optik sinir üzerine olan etkilerinin elektron mikroskobisi ile değerlendirilmesi
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Date
2023
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Hatay Mustafa Kemal Üniversitesi
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info:eu-repo/semantics/openAccess
Abstract
Amaç: Fluoksetin hidroklorür kullanımının karaciğer, testis, beyin gibi birçok dokuda oksidatif stresi indükleyerek hasar oluşturduğu yapılan çalışmalarda gösterilmiştir. Fluoksetinin oftalmolojik etkisi üzerine birkaç klinik çalışma dışında, deney hayvanı çalışması bulunmamaktadır. SSRI sınıfı bir antidepresan olan fluoksetin sinaptik aralıktaki serotonin düzeyini arttırır. Klinik çalışmalar artan serotonin düzeyine bağlı SSRI kullanımı sonucu optik nöropati oluşabileceğini öne sürmüştür fakat FLX'in optik sinire etkisini değerlendiren deney hayvanı çalışması bulunmamaktadır. FLX'in optik sinir üzerine bilinen en yaygın yan etkisi glokomdur. Çalışmamızda amacımız SSRI sınıfı bir antidepresan olan FLX'in optik sinir üzerine etkisini ultrastrüktüel olarak değerlendirmek ve literatüre yeni bir bakış açısı kazandırmaktır. Yöntem: Çalışmamızda kontrol ve deney olmak üzere iki ana grup bulunmaktadır. Kontrol grubuna (n=5) 4 hafta boyunca FLX'in çözücüsü %0.9'luk serum fizyolojik olduğu için serum fizyolojik intraperitoneal olarak verildi. Deney grubu için deneklere 4 hafta boyunca 10 mg/kg/gün fluoksetin hidroklorür intraperitoneal olarak uygulandı. 5 grup arasında istatistiksel olarak anlamlı farklılık elde edebilmek için Mead yöntemine göre hesaplama yapıldı ve her grupta minimum 5 sıçan ile çalışılması uygun görülmüş olup toplam 10 sıçan ile çalışıldı. Deney sonunda deneklerin optik sinirleri çıkarılıp elektron mikroskobik doku takibi yapıldı ve ince kesitler alındı. Alınan kesitler boyandıktan sonra elektron mikroskobik olarak incelendi ve her denekten 100 akson myelin kalınlığı, akson çapı, g oranı ve sinir lifi çapı olarak değerlendirildi. Bulgular: Kontrol grubu, deney grubu ile kıyaslandığında Elde edilen sonuca göre Akson Çapı (p=0,009), Kalınlık (p<0,001), Sinir Lifi Çapı (p<0,001) ve G Oranı (p=0,012) değişkenleri bakımından deney ve kontrol grubu arasında istatistiksel anlamlı farklılık olduğu görülmüştür. Kontrol grubuna oranla deney grubunda myelin kalınlığının, akson çapının, g oranın ve sinir lifi çapının istatiksel olarak anlamlı bir şekilde azaldığı saptanmıştır. Sonuç: SSRI sınıfına ait bir antidepresan olan fluoksetin hidroklorür kullanımının optik sinirde hasara neden olduğu, akson çapının, myelin kalınlığının, g oranının ve sinir lifi çapının azaldığı çalışmamızda gösterilmiştir. Yapılacak olan ileri çalışmalar ile bu hasarın mekanizması tam olarak anlaşılacaktır.
Background and Aim: Studies have shown that the use of fluoxetine hydrochloride causes damage by inducing oxidative stress in many tissues such as liver, testis and brain. Apart from a few clinical studies on the ophthalmological effect of fluoxetine, there are no experimental animal studies. Fluoxetine, an SSRI class antidepressant, increases the level of serotonin in the synaptic cleft. Clinical studies have suggested that optic neuropathy may occur as a result of the use of SSRIs due to increased serotonin levels, but there is no experimental animal study evaluating the effect of FLX on the optic nerve. The most common known side effect of FLX on the optic nerve is glaucoma. Our aim in our study is to evaluate the effect of FLX, an SSRI class antidepressant, on the optic nerve ultrastructurally and to bring a new perspective to the literature. Methods: There are two main groups in our study as control and experimental groups. The control group (n=5) was given saline intraperitoneally for 4 weeks because the solvent of FLX was 0.9% saline. For the experimental group, 10 mg/kg/day fluoxetine hydrochloride was administered intraperitoneally for 4 weeks. In order to obtain a statistically significant difference between the 5 groups, calculations were made according to the Mead method and it was deemed appropriate to work with a minimum of 5 rats in each group, and a total of 10 rats were studied. At the end of the experiment, the optic nerves of the subjects were removed, electron microscopic tissue follow-up was performed and thin sections were taken. After staining, the sections were examined electron microscopically and 100 axons from each subject were evaluated as myelin thickness, axon diameter, g ratio and nerve fiber diameter. Results: When the control group was compared with the experimental group, there was a statistical difference between the experimental and control groups in terms of Axon Diameter (p=0.009), Thickness (p<0.001), Nerve Fiber Diameter (p<0.001) and G Ratio (p=0.012) variables. significant difference was found. It was determined that myelin thickness, axon diameter, g ratio and nerve fiber diameter were statistically significantly decreased in the experimental group compared to the control group. Conclusion: It has been shown in our study that the use of fluoxetine hydrochloride, an antidepressant belonging to the SSRI class, causes damage to the optic nerve, and axon diameter, myelin thickness, g ratio and nerve fiber diameter are reduced. The mechanism of this damage will be fully understood with further studies. Key words: Optic nerve; Antidepresant; Axon; SSRI
Background and Aim: Studies have shown that the use of fluoxetine hydrochloride causes damage by inducing oxidative stress in many tissues such as liver, testis and brain. Apart from a few clinical studies on the ophthalmological effect of fluoxetine, there are no experimental animal studies. Fluoxetine, an SSRI class antidepressant, increases the level of serotonin in the synaptic cleft. Clinical studies have suggested that optic neuropathy may occur as a result of the use of SSRIs due to increased serotonin levels, but there is no experimental animal study evaluating the effect of FLX on the optic nerve. The most common known side effect of FLX on the optic nerve is glaucoma. Our aim in our study is to evaluate the effect of FLX, an SSRI class antidepressant, on the optic nerve ultrastructurally and to bring a new perspective to the literature. Methods: There are two main groups in our study as control and experimental groups. The control group (n=5) was given saline intraperitoneally for 4 weeks because the solvent of FLX was 0.9% saline. For the experimental group, 10 mg/kg/day fluoxetine hydrochloride was administered intraperitoneally for 4 weeks. In order to obtain a statistically significant difference between the 5 groups, calculations were made according to the Mead method and it was deemed appropriate to work with a minimum of 5 rats in each group, and a total of 10 rats were studied. At the end of the experiment, the optic nerves of the subjects were removed, electron microscopic tissue follow-up was performed and thin sections were taken. After staining, the sections were examined electron microscopically and 100 axons from each subject were evaluated as myelin thickness, axon diameter, g ratio and nerve fiber diameter. Results: When the control group was compared with the experimental group, there was a statistical difference between the experimental and control groups in terms of Axon Diameter (p=0.009), Thickness (p<0.001), Nerve Fiber Diameter (p<0.001) and G Ratio (p=0.012) variables. significant difference was found. It was determined that myelin thickness, axon diameter, g ratio and nerve fiber diameter were statistically significantly decreased in the experimental group compared to the control group. Conclusion: It has been shown in our study that the use of fluoxetine hydrochloride, an antidepressant belonging to the SSRI class, causes damage to the optic nerve, and axon diameter, myelin thickness, g ratio and nerve fiber diameter are reduced. The mechanism of this damage will be fully understood with further studies. Key words: Optic nerve; Antidepresant; Axon; SSRI
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Keywords
Göz Hastalıkları, Eye Diseases, Optik sinir; Antidepresan; Akson; SSRI
