College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
J Hazard Mater. 2023 Sep 15;458:131997. doi: 10.1016/j.jhazmat.2023.131997. Epub 2023 Jul 4.
As a third-generation neonicotinoid insecticide, dinotefuran is extensively used in agriculture, and its residue in the environment has potential effects on nontarget organisms. However, the toxic effects of dinotefuran exposure on nontarget organism remain largely unknown. This study explored the toxic effects of sublethal dose of dinotefuran on Bombyx mori. Dinotefuran upregulated reactive oxygen species (ROS) and malondialdehyde (MDA) levels in the midgut and fat body of B. mori. Transcriptional analysis revealed that the expression levels of many autophagy and apoptosis-associated genes were significantly altered after dinotefuran exposure, consistent with ultrastructural changes. Moreover, the expression levels of autophagy-related proteins (ATG8-PE and ATG6) and apoptosis-related proteins (BmDredd and BmICE) were increased, whereas the expression level of an autophagic key protein (sequestosome 1) was decreased in the dinotefuran-exposed group. These results indicate that dinotefuran exposure leads to oxidative stress, autophagy, and apoptosis in B. mori. In addition, its effect on the fat body was apparently greater than that on the midgut. In contrast, pretreatment with an autophagy inhibitor effectively downregulated the expression levels of ATG6 and BmDredd, but induced the expression of sequestosome 1, suggesting that dinotefuran-induced autophagy may promote apoptosis. This study reveals that ROS generation regulates the impact of dinotefuran on the crosstalk between autophagy and apoptosis, laying the foundation for studying cell death processes such as autophagy and apoptosis induced by pesticides. Furthermore, this study provides a comprehensive insight into the toxicity of dinotefuran on silkworm and contributes to the ecological risk assessment of dinotefuran in nontarget organisms.
作为第三代新烟碱类杀虫剂，呋虫胺被广泛应用于农业领域，其在环境中的残留对非靶标生物具有潜在影响。然而，呋虫胺暴露对非靶标生物的毒性效应在很大程度上尚不清楚。本研究探讨了亚致死剂量的呋虫胺对家蚕的毒性效应。呋虫胺可诱导家蚕中肠和脂肪体中活性氧（ROS）和丙二醛（MDA）水平升高。转录组分析表明，暴露于呋虫胺后，许多自噬和凋亡相关基因的表达水平发生显著改变，与超微结构变化一致。此外，自噬相关蛋白（ATG8-PE 和 ATG6）和凋亡相关蛋白（BmDredd 和 BmICE）的表达水平升高，而自噬关键蛋白（自噬体 1）的表达水平降低。这些结果表明，呋虫胺暴露可导致家蚕发生氧化应激、自噬和凋亡。此外，其对脂肪体的影响明显大于对中肠的影响。相反，自噬抑制剂预处理可有效下调 ATG6 和 BmDredd 的表达水平，但诱导自噬体 1 的表达，表明呋虫胺诱导的自噬可能促进凋亡。本研究揭示了 ROS 生成调节了呋虫胺对自噬和凋亡之间相互作用的影响，为研究农药诱导的自噬和凋亡等细胞死亡过程奠定了基础。此外，本研究为家蚕对呋虫胺的毒性提供了全面的认识，并有助于对非靶标生物中呋虫胺的生态风险进行评估。
