The potential endocrine disruption of neonicotinoids poses a significant threat to the survival of small farmland lizards. We systematically evaluated the distribution, metabolism, and toxicity of three neonicotinoids (dinotefuran, thiamethoxam, and imidacloprid) in the Eremias argus during a 35-day oral administration exposure. Lizards could quickly transfer and store neonicotinoids into the scale and eliminated through molting. Dinotefuran was most prone to accumulation in lizard tissues, followed by thiamethoxam, and imidacloprid was generally present in the form of its terminal metabolite 6-chloropyridinyl acid. Exposure to dinotefuran resulted in hepatic oxidative stress damage, decreased plasma growth hormone concentration, and down-regulation of ghr, igf1 and igfbp2 gene expression. These indicated that dinotefuran might have potential growth inhibition toxicity to lizards. Although imidacloprid caused severe liver oxidative stress damage, the effect of imidacloprid on GH/IGF axis was not obvious. Compared to dinotefuran and imidacloprid, thiamethoxam had the least damage to liver and minimal impact on GH/IGF axis. This study verified the possible damage of neonicotinoids to lizard liver and the interference of GH/IGF axis for the first time.
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