Chlorfenapyr (CHL) is a type of insecticide with a wide range of insecticidal activities and unique targets. The extensive use of pesticides has caused an increase in potential risks to the environment and human health. However, the potential toxicity of CHL and its mechanisms of action on humans remain unclear. Therefore, human liver cells (HepG2) were used to investigate the cytotoxic effect and mechanism of toxicity of CHL at the cellular level. The results showed that CHL induced cellular toxicity in HepG2 cells and induced mitochondrial damage associated with reactive oxygen species (ROS) accumulation and mitochondrial calcium overload, ultimately leading to apoptosis and autophagy in HepG2 cells. Typical apoptotic changes occurred, including a decline in the mitochondrial membrane potential, the promotion of Bax/Bcl-2 expression causing the release of cyt-c into the cytosol, the activation of cas-9/-3, and the cleavage of PARP. The autophagic effects included the formation of autophagic vacuoles, accumulation of Beclin-1, transformation of LC3-II, and downregulation of p62. Additionally, DNA damage and cell cycle arrest were detected in CHL-treated cells. These results show that CHL induced cytotoxicity associated with mitochondria-mediated programmed cell death (PCD) and DNA damage in HepG2 cells.
Buprofezin (BUP) is an insecticide used for control of sucking pests. Its widespread use has raised concerns about possible adverse effects on the environment, and especially human health. The mechanism of toxicity of BUP, with respect to human health, is still unclear. Consequently, human A549 cells were employed to clarify the cytotoxicity and toxic mechanism of BUP at the molecular and cellular levels. The outcomes revealed BUP latent toxicity to A549 in a time- and dose-related way. Moreover, BUP induced mitochondrial dysfunction associated with mitochondrial membrane potential collapse, mitochondrial calcium overload, and ROS aggregation, ultimately resulting in the apoptosis and autophagy of A549 cells. Symbolic apoptotic and autophagic modifications were detected, including leakage of cyt-c, elevation of Bax/Bcl-2, activation of cas-9/-3, constitution of autophagic vacuoles, promotion of Beclin-1, conversion of LC3-II, and reduction of p62. Additionally, in total, 1216 differentially expressed genes (DEGs) were defined after BUP treatment. Several apoptosis- and autophagy-related genes, such as BCL2, ATG5, and ATG16, down- or upregulated at the RNA transcription level, and functional DEGs enrichment analysis showed their involvement in the metabolism of xenobiotics by cytochrome P450, mTOR signalling pathway, and AMPK signalling pathway. Results confirmed that BUP could induce cytotoxicity associated with mitochondria-mediated programmed cell death in A549 cells.
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