Spiromesifen Metabolite M01

As a promising acaricide and potentially hazardous material, the defense mechanisms of non-target organisms to its exposure are unknown. This study investigates the bioavailability and biotoxicity of spiromesifen and spiromesifen-enol (M01), its main metabolite, in Eisenia fetida. The results showed that M01 was more persistent in the soil environment and E. fetida than spiromesifen. Transcriptome analysis indicated that the spiromesifen- and M01-induced differentially expressed genes (DEGs) were mainly enriched in lysosomal and phagosomal pathways. Analysis of the key common DEGs showed that both spiromesifen and M01 significantly influenced the lysosomes, phagosomes, antioxidant systems, and detoxification systems. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) showed that spiromesifen and M01 damaged E. fetida epidermis and enhanced lysosomal and phagosomal activities. Significant oxidative stress effects were observed at the end of exposure. The hydroxyl free radical (·OH-) content and neutral red retention time (NRRT) could serve as sensitive early biomarkers to predict their pollution. These results revealed the synergistic effects of the epidermis, lysosomes, phagosomes, antioxidant systems, and detoxification system in resisting spiromesifen- and M01-induced damage, which could contribute to the defense mechanisms of non-target organisms against these pollutants.