Yılmaz, ErcanGül, MehmetMelekoğlu, RaufTürköz, YusufÖzyalın, FatmaParlakpınar, Hakan2019-07-182019-07-182018Yılmaz, E. Gül, M. Melekoğlu, R. Türköz, Y. Özyalın, F. Parlakpınar, H. (2018). Cilt:33 Sayı:4, 306-313 ss.https://hdl.handle.net/11616/12727Purpose: To Investigate the cause of congenital anomalies resulted from gestational diabetes on fetal cardiac tissue in experimental animal study model. Methods: Totally 12 female WIstar albino rats were divided Into two groups, each consisting of 6 rats. Streptozotocln (60 mg/kg) was administered intraperltoneally to the study group by dissolving In citrate solution. The rats with a blood glucose level of 200 mg/dL and above were considered to be diabetic rats. Total antioxidant status (TAS), total oxidative stress (TOS) and oxidative stress Index (OSI) values were calculated In the cardiac tissues and maternal serum samples of the fetuses delivered by cesarean section after the mating process. The cardiac tissues were also subjected to hlstopathologlcal examination. Results: TOS and OSI values In fetal cardiac tissues of the diabetic rats were found to be significantly higher than that of the control group (p=0.026 and p=0.005). Histopathological examination revealed that the mitotic Index was lower and the cell organization was found to be damaged In the fetuses of the study group rats. Conclusion: Increased levels of free oxygen radicals considered to be due to hyperglycemia may cause congenital anomalies, especially during organogenesis period, by disrupting cell homeostasis and adversely affecting mitosis.eninfo:eu-repo/semantics/openAccessOxıdatıve StressSerum-LevelsMedıatorsArticle33430631310.1590/s0102-865020180040000002