Speaker
Description
Abstract
The most severe congenital abnormalities are known as neural tube defects (NTDs),
which are characterized by defective neural tube closure during early development.
The present study investigates the embryo-toxic effect of serotonin and cadmium
chloride and the ability of folic acid and inositol to exert a neuroprotective effect in
an in vivo model based on fertilized chick embryos (Gallus gallus domesticus).
Fourteen eggs were assigned to graded serotonin exposure of 10, 25, and 50 µL, fixed
cadmium chloride of 10 µL, and also co-treated with folic acid at 50 µL or inositol at
100 µL. Embryos were incubated for 48–72 hours, harvested, and examined for
survival and gross structural changes. The outcome indicated that serotonin and
cadmium chloride induced dose-dependent developmental abnormalities, comprising
notches in the neural tube, notochord-brain separation, and spina bifida-like
development. Combined exposure was embryonic lethal. Folic acid was able to
prevent damage in lower dose groups but not with high serotonin. Inositol was not
protective and all the inositol-treated embryos failed to develop. The results illustrate
the dose sensitivity of embryonic tissues to teratogens and show the preeminent
importance of folic acid. Inositol might need co-factors or combination therapy to be
effective.
This study provides experimental evidence for prenatal screening, medically
controlled use of drugs, and nutritional supplementations during pregnancy.
Key words: Neural tube defects (NTDs), Teratology, Chick embryo model (Gallus
gallus domesticus), Serotonin, Cadmium chloride (heavy metal), Folic acid, Inositol,
Neurodevelopment, Embryo-toxicity, Neuroprotection, Anencephaly, Spina Bifida
Cystica, Meningocele, Encephalocele, Myelocele, and Meningomyelocele.
