Investigation of the Effect of Tenoxicam on Neural Tube Defect Using Chick Embryo Model

Area of Science:

• Developmental biology
• Teratology
• Neuroembryology

Background:

• Neural tube defects (NTDs) are common congenital abnormalities.
• Understanding the teratogenic potential of non-steroidal anti-inflammatory drugs (NSAIDs) like tenoxicam is crucial for prenatal safety.
• Early embryonic development, particularly neural tube closure, is a sensitive period for teratogenic insult.

Purpose of the Study:

• To investigate the teratogenic effects of tenoxicam on embryonic neural tube formation.
• To determine if tenoxicam induces neural tube defects (NTDs) in a dose-dependent manner.
• To explore potential mechanisms underlying tenoxicam-induced embryonic damage.

Main Methods:

• A windowing technique was used to access 100 fertile chicken embryos after 24 hours of incubation.
• Embryos were divided into four groups and administered varying doses of tenoxicam (0.01, 0.02, 0.10 μg) or a control solution.
• Sub-blastodermal administration of 20 μL tenoxicam solution was followed by 24 hours of further incubation, with evaluation at 48 hours.

Main Results:

• Tenoxicam exposure resulted in a dose-dependent increase in neural tube closure defects.
• Group 3 (0.10 μg) showed the highest incidence of NTDs (9 out of 25 embryos), while Group 1 (0.01 μg) had the lowest (2 out of 25).
• Rates of absent embryonic development were 8%, 8%, 12%, and 4% for tenoxicam doses of 0.01, 0.02, 0.10 μg, and the control group, respectively.

Conclusions:

• Tenoxicam induces midline closure defects in early chicken embryos in a dose-dependent manner.
• The findings suggest potential teratogenic risks associated with tenoxicam exposure during critical developmental windows.
• Further research is needed to elucidate the precise mechanisms of tenoxicam-induced embryonic damage and to develop strategies for preventing congenital defects.