Ipconazole (IPC) is a chiral triazole fungicide and commonly used for disease control in seeds. This study investigated the bioactivity and potential mechanism of ipconazole against pathogenic microorganisms at the chiral perspective. It explored the accumulation behavior of ipconazole enantiomers within the soil-earthworm system and evaluated its toxic effects on earthworms. Bioactivity evaluation revealed that the bioactivity order of ipconazole against three plant pathogens is (-)-1S,2 R,5S-IPC > rac-IPC > (+)-1R,2S,5R-IPC, and the bioactivity of (-)-1S,2 R,5S-IPC is 34.6-129.5 times higher than that of (+)-1R,2S,5R-IPC. Molecular docking found that (-)-1S,2 R,5S-IPC has a stronger binding affinity for the target protein CYP51 to cause activity differences. Accumulation and metabolism studies revealed that (-)-1S,2 R,5S-IPC is more persistent than that of (+)-1R,2S,5R-IPC, and ipconazole was primarily metabolized into hydroxylated ipconazole through hydroxylation in the soil-earthworm system. Toxicological evaluation found growth inhibitory effects and histopathological damage to earthworms at an exposure concentration of 1.5 mg kg(-1) ipconazole. Further investigation indicated that these toxic effects of ipconazole were caused by inducing oxidative damage and influencing the functional gene expression of related growth. These research findings will further enhance the understanding of the activity and risks of ipconazole enantiomers, contributing to the safer use of ipconazole in the agricultural environment.

Penthiopyrad, a chiral pesticide, has been widely used in agricultural production. However, systematic evaluation of stereoselective bioactivity and biotoxicity of penthiopyrad in soil environment is insufficient. In this study, the stereoselective bioactivity of penthiopyrad against three soil-borne disease pathogens and its stereoselective biotoxicity to soil non-target organisms were investigated. The present results showed that the bioactivities of S-penthiopyrad were 546, 76 and 1.1-fold higher than those of R-penthiopyrad due to their different interaction modes with SDH in different target pathogens. S-penthiopyrad was more persistent in the soil environment and had stronger bioaccumulation than R-penthiopyrad. The accumulation of penthiopyrad in earthworms induced the response of detoxification system, resulting in the significant increases in the activity of detoxifying enzymes, such as GST, CarE, and CYP450. Additionally, both S-penthiopyrad and R-penthiopyrad induced cell apoptosis, intestinal damage and differentially expressed genes in earthworms, especially S-penthiopyrad. Furthermore, S-penthiopyrad has stronger binding capacity with COL6A and ACE proteins, while Rpenthiopyrad has stronger binding capacity with CYP450 family proteins, which may be the main reason for the differences in biotoxicity between PEN enantiomers. Considering the differences in bioactivity and biotoxicity of penthiopyrad enantiomers, as well as the modes of action of pesticides on target and non-target organisms, Spenthiopyrad has greater potential for future development.

Continued application of new chiral fungicide mefentrifluconazole (MFZ) increases its risk to soil ecosystem. However, the toxicity of MFZ enantiomers to soil fauna and whether stereoselectivity exists remains poorly elucidated. Based on multilevel toxicity endpoints and transcriptomics, we investigated the negative effects of racemic, R-(-)-, and S-(+)-MFZ on Eisenia fetida. After exposure to S-(+) configuration at 4 mg/kg for 28 day, its reactive oxygen species levels were elevated by 15.4% compared to R-(-) configuration, inducing enantiospecific oxidative stress and transcriptional aberrations. The S-(+) isomer induced more severe cell membrane damage and apoptosis than the R-(-) isomer, and notably, the selectivity of apoptosis is probably dominated by the mitochondrial pathway. Mechanistically, differential mitochondrial stress lies in: S-(+) isomer specifically upregulated mitochondrial cellular component compared to R-(-) isomer and identified more serious mitochondrial fission. Furthermore, S-(+) conformation down -regulated biological processes associated with ATP synthesis and metabolism, with specific inhibition of mitochondrial respiratory electron transport chain complex I and IV activity resulting in more severe electron flow disturbances. These ultimately mediated enantioselective ontogenetic process disorders, which were supported at phenotypic (weight loss), genetic, and protein (reverse modulate TCTP and Sox2 expression) levels. Our findings offer an important reference for elucidating the enantioselective toxicological mechanism of MFZ in soil fauna.