Spinosad is one of the most extensively used bio-pesticide in the world. The effects of pesticide in human health are mainly associated with its residue in food or occupational exposure in agricultural production. The lung is the direct target of pesticides exposure, although the study of inhalation damage caused by Spinosad remains unclear. The aim of the present study was to evaluate the cytotoxic effects of the Spinosad in human lung cells. We demonstrated that Spinosad could inhibite the proliferation of human lung epithelial A549 cells, induce the DNA damage and enhance the programmed cell death. Intracellular biochemical assay indicated that DNA double strand breaks, cleaved of PARP, release of cytochrome c, decrease of mitochondrial membrane potential, generation of reactive oxygen species (ROS), activation of caspase-3/9, increase of Bax/Bcl-2 ratio, LC3-II conversion, accumulation of Beclin-1, degradation of p62 and the changes in the phosphorylation of AMPK, mTOR are contributed to the toxic effects of Spinosad in A549 cells. The results showed that the cytotoxicity of Spinosad may be associated with the activity of mitochondrial apoptotic pathways or AMPK/mTOR-mediated autophagy. Meanwhile, the DNA stand breaks caused by the Spinosad suggest it has a potential genotoxic effects on human lung cells. We conclude that Spinosad has a potential risk to human health by inducing the cytotoxic effects.
Keywords: AMPK/mTOR-mediated autophagy; Cytotoxicity; DNA damage; Human epithelial A549 lung cells; Spinosad.
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