The study aimed to explain the crosstalk of cerebral cortex neuron cell death due to the carbofuran exposure during the embryonal development. This experimental laboratory study used 81 fetuses from 27 mice mothers and carbofuran were exposed in gavage manner at the pregnancy age of 6-15 days old at a dose of 0.0417mg/Kg body weight and 0.0208mg/Kg body weight. On the 17th day of pregnancy, the mice mothers were terminated and its fetal cerebrums were measured for its ROS activity such as the malondialdehyde/MDA levels and superoxide dismutase/SOD activity and examined its cerebral cortex neuron cells which included the apoptosis (tunnel assay) and necrosis (HE staining). The examination of p53 and caspase 3 used the immunohistochemistry. This study concluded that there was moderate in these relationships between carbofuran doses and MDA and p53 levels; and between SOD activity and MDA and P53 levels; and between p53 and caspase 3, apoptotic and necrotic cells. Meanwhile, both relationships between carbofuran doses and SOD activity and between caspase 3 and apoptotic cells were strong. Furthermore, there was no any relationship between MDA levels and necrotic cells. The expression of p53, caspase 3 and apoptotic cells showed that carbofuran could increase the embryonal cerebral ROS activity and injure the core DNA which caused the apoptosis via intrinsic pathways through p53 or mitochondria. MDA levels did not increase any damage to the cell membrane system and cause necrosis. There was a relationship between necrotic cells and p53 due to a decrease in mitochondrial function for producing energy. Apoptotic and necrotic neuron cells occurred because p53 opened the opportunities for prevention and treatment of the ROS activities’ effects due to the carbofuran exposure during pregnancy.
- Mus musculus