E-ISSN: 1019-5157
ISSN: 2651-5024
Research
The Teratogenic Effects of Sodium Acid Pyrophosphate on Neural Tube Development in the Chick Embryo
Sarper Kocaoğlu✉ ,
Eyüp Çetin ,
Halime Tuba Canbaz ,
Selin Ursavaş ,
Murat Yücel ,
Emine Demir ,
Selin Tural
Neurosurgery, Health Science University Haydarpaşa Numune Training and Research Hospital; Neurosurgery, Haydarpaşa Numune Training andResearchHospital
DOI: 10.5137/1019-5149.JTN.50975-26.4
Accepted: 04/06/2026
Article in Press
Corresponding Author:
Sarper Kocaoğlu (drsarperkocaoglu@gmail.com)
Abstract
Aim
Sodium acid pyrophosphate is a phosphate-based food additive used in several processed food products. However, its potential effects on early neural development have not been sufficiently investigated. In this experimental study, we evaluated whether sodium acid pyrophosphate exposure during early neurulation affects embryo survival and neural tube closure in a chick embryo model.
Material and Methods
Fertilized specific pathogen-free chicken eggs were assigned to three groups: control, 1% sodium acid pyrophosphate, and 10% sodium acid pyrophosphate, with 20 eggs in each group. After 30 hours of incubation, corresponding approximately to Hamburger-Hamilton stage 9, the eggs were windowed, and 0.1 mL of distilled water or sodium acid pyrophosphate solution was injected beneath the embryonic disc. The embryos were incubated until 72 hours of development. Survival was evaluated according to the presence of cardiac activity and intact vascularization. Surviving embryos were then dissected, fixed in 10% formalin, processed for routine paraffin histology, stained with hematoxylin and eosin, and examined for neural tube closure defects.
Results
All control embryos survived and showed normal neural tube development. In both sodium acid pyrophosphate-exposed groups, survival decreased to 50%, compared with 100% in the control group. Among surviving embryos, neural tube defects were observed in 7 of 10 embryos in the 1% group and in all 10 surviving embryos in the 10% group. Defects in the 1% group were generally localized, whereas embryos exposed to 10% sodium acid pyrophosphate showed more extensive cranial and caudal closure abnormalities. Histopathological examination supported the gross morphological findings and demonstrated disrupted neural fold fusion and altered neuroepithelial organization in affected embryos.
Conclusion
Under the experimental conditions of this study, high-dose sodium acid pyrophosphate exposure was associated with reduced embryo survival and an increased frequency of neural tube defects in chick embryos. Because the concentrations used represent exploratory high-dose experimental exposure, these findings should be interpreted as preliminary hazard-identification data rather than direct evidence of risk under normal dietary intake conditions. Further dose-ranging and mechanistic studies are needed to clarify the developmental relevance of sodium acid pyrophosphate under more physiologically relevant exposure conditions.
Sodium acid pyrophosphate is a phosphate-based food additive used in several processed food products. However, its potential effects on early neural development have not been sufficiently investigated. In this experimental study, we evaluated whether sodium acid pyrophosphate exposure during early neurulation affects embryo survival and neural tube closure in a chick embryo model.
Material and Methods
Fertilized specific pathogen-free chicken eggs were assigned to three groups: control, 1% sodium acid pyrophosphate, and 10% sodium acid pyrophosphate, with 20 eggs in each group. After 30 hours of incubation, corresponding approximately to Hamburger-Hamilton stage 9, the eggs were windowed, and 0.1 mL of distilled water or sodium acid pyrophosphate solution was injected beneath the embryonic disc. The embryos were incubated until 72 hours of development. Survival was evaluated according to the presence of cardiac activity and intact vascularization. Surviving embryos were then dissected, fixed in 10% formalin, processed for routine paraffin histology, stained with hematoxylin and eosin, and examined for neural tube closure defects.
Results
All control embryos survived and showed normal neural tube development. In both sodium acid pyrophosphate-exposed groups, survival decreased to 50%, compared with 100% in the control group. Among surviving embryos, neural tube defects were observed in 7 of 10 embryos in the 1% group and in all 10 surviving embryos in the 10% group. Defects in the 1% group were generally localized, whereas embryos exposed to 10% sodium acid pyrophosphate showed more extensive cranial and caudal closure abnormalities. Histopathological examination supported the gross morphological findings and demonstrated disrupted neural fold fusion and altered neuroepithelial organization in affected embryos.
Conclusion
Under the experimental conditions of this study, high-dose sodium acid pyrophosphate exposure was associated with reduced embryo survival and an increased frequency of neural tube defects in chick embryos. Because the concentrations used represent exploratory high-dose experimental exposure, these findings should be interpreted as preliminary hazard-identification data rather than direct evidence of risk under normal dietary intake conditions. Further dose-ranging and mechanistic studies are needed to clarify the developmental relevance of sodium acid pyrophosphate under more physiologically relevant exposure conditions.
Keywords
chicken embryo
sodium acid pyrophosphate
food additives
neural tube defect
histopathology