Transcriptome analysis reveals the molecular mechanisms of neonicotinoid acetamiprid in Leydig cells.

This article focuses on investigating the molecular mechanisms underlying the reproductive toxicity of acetamiprid (ACE), a widely used neonicotinoid insecticide, in TM3 Leydig cells. The study found that ACE exposure reduces cell viability and induces apoptosis in a time- and dose-dependent manner, with transcriptome analysis revealing 1,477 differentially expressed genes related primarily to DNA replication and cell cycle processes. Validation by qPCR indicated that ACE may promote G1/S and G2/M cell cycle arrest through altered expression of key genes such as Mdm2, Cdkn1a (p21), Gadd45, and various cyclins, implicating the involvement of p53, FoxO, and HIF-1 signaling pathways as well as ferroptosis in ACE-induced cytotoxicity. These findings provide a theoretical foundation for further in vivo and in vitro studies on the non-target reproductive toxicity mechanisms of neonicotinoid insecticides.