Bu çalışmanın amacı, C vitamininin Leydig (TM3) hücrelerinde glisidamid kaynaklı sitotoksisite, oksidatif stres ve apoptoz üzerindeki rolünü ortaya çıkarmaktır. Leydig hücreleri 24 saat boyunca glisidamid (1, 10, 100 ve 1000 μM) ve / veya C vitamini (50 μM) ile muamele edilmiştir. Deney süresinin tamamlanmasından sonra, Leydig hücrelerinde hücre canlılığı, laktat dehidrogenaz enzimi miktarı, apoptoz-nekroz oranları, hidroksil radikali, hidrojen peroksit ve lipit peroksidasyonu gibi oksidatif stres parametrelerinin seviyeleri belirlendi. Sonuçlar glisidamid uygulamasının yüksek konsantrasyonda (1000 μM) önemli ölçüde Leydig hücre canlılığını azalttığını ve sitotoksisitenin arttığını gösterdi. Ayrıca, glisidamid reaktif oksijen türlerinin ve lipid peroksidasyonunun üretimini önemli ölçüde arttırarak oksidatif hasara yol açmıştır. Glisidamide maruz kalma, Leydig hücrelerinde erken apoptoz, apoptoz ve nekroz oluşumunu artırmıştır. Sonuç olarak, glisidamid lipit peroksidasyonuna ve Leydig hücrelerinde reaktif oksijen türlerinin oluşmasına bağlı apoptosise neden olmuş, C vitamininin ise glisidamidin neden olduğu toksisiteye karşı iyileştirici bir rolü olduğu gösterilmiştir.

THE EFFECTS OF VITAMIN C ON GLYCIDAMIDE-INDUCED CELLULAR DAMAGE AND APOPTOSIS IN MOUSE LEYDIG CELLS

The aim of this study was to elucidate the role of vitamin C on glycidamide-induced cytotoxicity, oxidative damage and cell death in Leydig (TM3) cells. Leydig cells were exposed to glycidamide (1, 10, 100 and 1000 μM) and/or vitamin C (50 μM) for 24 h. After completion of the exposure time, cell viability, amount of lactate dehydrogenase enzyme, apoptosis-necrosis rates, levels of oxidative stress parameters such as hydroxyl radical, hydrogen peroxide and lipid peroxidation were determined in Leydig cells. The results showed that glycidamide administration decreased Leydig cell viability and increased cytotoxicity significantly at high concentration (1000 μM). In addition, glycidamide generated oxidative damage by significantly increasing the production of reactive oxygen species and lipid peroxidation. Exposure to glycidamide increased the formation of early apoptosis, apoptosis and necrosis in Leydig cells. Consequently, glycidamide has been shown to cause apoptosis due to lipid peroxidation and formation of reactive oxygen species in Leydig cells, and vitamin C has a therapeutic role against toxicity caused by glycidamide.

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