Prenatal lead acetate exposure induces apoptosis and changes GFAP expression during spinal cord development

Lead is an important heavy metal pollutant in the environment, and it induces neurodevelopmental toxicity, which is characterized by histological, ultrastructural, and neurochemical changes in the central nervous system. The aim of this study was to evaluate the effects of prenatal acute lead exposure on apoptosis, GFAP expression, and lead deposition in the developing spinal cord. Chick embryos were exposed to 150 μg or 450 μg doses of lead acetate via yolk sac at E3 or E5 embryonic ages and incubated for six days. Lead deposition was observed in the ependymal cells, developing dorsal, and ventral horns, and in the white matter of all the exposed embryos. TUNEL-positive cells were found in all layers of the spinal cord of the control and treated embryos, and lead exposure resulted in a significant increase in the numerical density of the apoptotic cells. Control embryos showed intense GFAP expression in the ependymal cells of the roof and floor plates, and in the gray and white matters; whereas exposure to lead reduced GFAP reactivity. In ovo lead exposure induces apoptosis, and reduces GFAP expression in the nervous system of the chick embryos, which may cause impairments during neuronal development and consequences in childhood and adulthood.

► Lead impregnates in the embryonic spinal cord layers after in ovo exposure.
► In ovo lead exposure induces apoptosis in neuronal and glial cells of the spinal cord.
► Lead causes GFAP downregulation in the spinal cord during embryonic development.