Interaction between autophagy, apoptosis and necrosis of infant mice (MUS musculus) brain cells from its carbofuran exposed mothers during lactation periods

This study aimed to determine the mechanism of autophagy, apoptosis and necrosis in the neurons of infant mice (Mus musculus) whose mothers were exposed to carbofuran during the lactation period. This experimental study included 20 mice; carbofuran was administered at 0.625LD₅₀ fractionsmg/kg BWby (1/8gavageLDto),miceand at0.3125the dosesmg/kgofBW1.25(1/16mg/kgLDbody). Mothersweight (BW)were exposed(1/4 LD₅₀to), carbofuran during lactation⁵⁰on Days 1–9. On Day 10, infant mice⁵⁰ were sacrificed in order to determine the number of neuron cells expressing protein kinase B (Akt) and the mammalian target of rapamycin complex 1 (mTORC1) as autophagy pathway using immunohistochemistry, apoptosis using the Tunel Assay, and necrosis using haematoxylin and eosin staining. The results of Akt, mTORC1, apoptosis, and cell necrosis were analyzed by analysis of variance (ANOVA) and Duncan tests. The results of the study showed that exposing the mothers to carbofuran during lactation caused an increase in necrosis and apoptosis of neuronal cells but did not cause autophagy in neuron cells via the Akt/mTOR pathway of infant mice. The increase in apoptotic neurons opens up opportunities for the prevention and handling of the effects of reactive oxygen species activities due to carbofuran exposure during lactation periods.