Effect of arsenic on neural tube in mouse embryo and relation to reduced folate carrier (RFC-1)

Arsenic is an important environmental toxicant which is usually found in drinking water in inorganic form. The hypothesis tested in this investigation is; arsenic exposure causes neural tube defects (NTDs) and these defects of the central nervous system are more likely related to folate deficiency during fetal life. In this study, sodium arsenate was administered via intraperitoneal route at a rate of 40 mg/kg body weight on the 6th day of gestation to every individual of 20 mated Albino mice. On the 8th (E8), 10th (E10), 16th (E16) and 19th (E19) days of the gestation, the pregnant mice in control and experimental groups were sacrificed by cervical dislocation. All embryos belonging to (E16) and (E19) were examined for external morphological neural tube defects. Histological staining techniques were haematoxylin and eosin and the immunofluorescence staining was also implemented. It was observed that, the intraperitoneal injection of sodium arsenate caused a number of morphological neural tube defects including; open fourth ventricle, exencephally, myelomeningocele and anencephaly. Difference in control and experimental specimens was significant (P<0.001) on the (E16) group. The histomorphologic changes of neural tube were significant in all of the experimental groups in comparison to the controls. Immunofluorescence study revealed reduced folate carrier (RFC-1) protein reduction in neural tissue, and these results demonstrate that the association between prenatal exposure to inorganic arsenic and NTDs is more likely related to a defect in reduced folate carrier protein.