Akademik Veri Yönetim Sistemi
Turkish Neurosurgery, cilt.34, sa.5, ss.827-832, 2024 (SCI-Expanded)
AIM: To evaluate tenoxicam’s effects on embryonic neural tube formation to identify potential teratogenicity and determine the underlying mechanisms leading to neural tube defects (NTDs). MATERIAL and METHODS: This study was conducted at our University’s Neuro-embryology Laboratory. A total of 100 fertile chicken eggs were opened using the windowing method after 24 hours of incubation. The embryo models were divided into four groups based on tenoxicam dosage: 0.01, 0.02, 0.10 μg, and control group (0.9% SF was administered). The tenoxicam groups were administered 20 µL volume sub-blastodermally. The eggs were incubated for another 24 hours after being covered with sterile draping. All the eggs were opened at the 48th hour, and the embryos were evaluated. RESULTS: Each group consisted of 25 chicken embryos. Normal neural tube development was observed in Group 1 (0.01μg) with 23 out of 25 embryos, Group 2 (0.02 μg) with 20 out of 25 embryos, Group 3 (0.10μg) with 16 out of 25 embryos, and Group 4 (control group) with 24 out of 25 embryos. Additionally, the rates of absence of embryo development were 8%, 8%, 12%, and 4% in Groups 1, 2, and 3 and the control group, respectively. CONCLUSION: We observed that tenoxicam use caused midline closure defects in early chicken embryos in a dose-dependent manner. Further studies are required to determine the mechanisms underlying the embryonic damage and teratogenic effects due to genetic and environmental factors and minimize the development of congenital defects.