Abstract：
The novel pesticide chlorantraniliprole (CAP) is widely used for pest control in agriculture, and the safety for non-target organisms of trace residues in the environment has received widespread attention. In the present study, exposure to low concentrations of CAP resulted in abnormal silk gland development in the B. mori, and induced the release of intracellular Ca2+ in addition to the triggering of Ca2+-dependent gene transcription. Moreover, the CAP treatment group exhibited down-regulation of oxidative phosphorylation and antioxidant enzyme-related genes in the silk gland, resulting in peroxide accumulation. Furthermore, transcript levels of autophagy-related genes were significantly up-regulated and protein levels of LC3-I and LC3-II were up-regulated, indicating an increase in autophagy. The protein levels of ATG5 and NtATG5 were also significantly up-regulated. While the protein levels of caspase3 and active caspase3 were significantly up-regulated consistent with the transcript levels of key genes in the apoptotic signaling pathway, ultimately affecting silk protein synthesis. Overall, these findings indicate that low concentration CAP induced abnormal development in the silk gland of B. mori by causing intracellular Ca2+ overload, which inhibits oxidative phosphorylation pathway and the removal of reactive oxygen species, leading to a driving a shift from autophagy to apoptosis. The findings herein provided a basis for evaluating the safety of CAP environmental residues on non-target organisms.
摘要：
新型农药chloantraniliprole（CAP）被广泛用于农业中的病虫害防治。环境中微量残留的非靶标生物的安全性受到了广泛的关注。在本研究中,暴露于低浓度的CAP导致在B.mori中异常的丝腺发育，除了触发Ca2依赖性基因转录外，还诱导了细胞内Ca2的释放。此外，CAP处理组表现出丝腺中氧化磷酸化和抗氧化酶相关基因的下调，导致过氧化物积累。此外，自噬相关基因转录水平显著上调，LC3-I和LC3-II蛋白水平上调，表明自噬增加。ATG5和NtATG5的蛋白质水平也显著上调。虽然caspase3和活性caspase3的蛋白水平显著上调，与凋亡信号通路中关键基因的转录水平一致，最终影响蚕丝蛋白的合成。总的来说,这些发现表明，低浓度CAP通过引起细胞内Ca2+过载，在桑树丝腺中引起异常发育，抑制氧化磷酸化途径和活性氧的去除，导致驱动从自噬到凋亡的转变。本文的发现为评估CAP环境残留物在非目标生物体上的安全性提供了基础。
