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Introduction The aim of the study was to describe the process of neuron death in the cerebral cortex caused by embryonic carbofuran exposure. Material and Methods 81 mouse foetuses from 27 breeding mice were used in the study. Carbofuran was administered by gavage from the 6 th  to the 15 th  day of gestation to two groups: one at 0.0208 and the other at 0.0417 mg/kg b.w. On the 17 th  day, the mice were sacrificed and the foetuses were taken to measure the ROS (malondialdehyde/MDA and superoxide dismutase/SOD) activity in brain tissue, the number of apoptotic embryonic cerebral cortex neurons using a TUNEL assay, and necrotic cells using HE staining. Examination of p53 and caspase 3 expression was done by immunohistochemistry. Data were analysed using analysis of variance (ANOVA) and Duncan’s test. Results Increased activity of cerebral ROS characterised by significant elevation of the MDA level (P &lt; 0.05), decreased SOD (P &lt; 0.01), increased p53 and caspase 3 expression, and cerebral cortical neuron death either by necrosis or apoptosis (P &lt; 0.05) were found. At the low dose carbofuran increased expression of p53, caspase 3, and apoptosis. At the high dose it increased levels of MDA and necrosis. Conclusion Increased expression of p53 and caspase 3 and apoptosis indicated that carbofuran may cause apoptosis through the intrinsic pathway. The increased apoptosis grants an opportunity to prevent and treat the effect of ROS due to gestational carbofuran exposure.

Mouse (Mus musculus) embryonic cerebral cortex cell death caused by carbofuran insecticide exposure