Integrated Multi-Omics Analysis Reveals the Mechanism of Haloxyfop-P-methyl Residue Suppressing Seed Germination in...

Haloxyfop-P-methyl (HPM) is widely used for grass weed control in oilseed rape production. However, whether its residues affect subsequent seed germination and the underlying mechanisms remains unclear. In this study, seeds harvested from HPM-treated fields exhibited a significantly reduced germination rate of 36.5%, compared with 100% in the control group, accompanied by abnormal cell morphology. Residue analysis revealed an HPM concentration of 3.36 mg kg^-1 in the treated seeds, exceeding the Chinese maximum residue limit (MRL) of 3 mg kg^-1 (GB 2763). Given that herbicides often induce oxidative stress, we measured a range of antioxidant markers (H₂O₂, MDA, SOD, POD, GSH, GSSG, AsA, and DHA) during germination (12 h and 24 h) but detected no significant changes, which did not support oxidative stress as the primary mechanism during this phase. Relative electrical conductivity measurements further indicated that membrane integrity was already compromised in dry seeds, suggesting that oxidative injury-if it occurred-may have taken place during seed development rather than during germination. To elucidate the molecular basis, we performed transcriptomic, metabolomic, and lipidomic analyses, which revealed significant downregulation of fatty acid biosynthesis genes and marked alterations in the lipidome profile. Collectively, our multi-stage investigation demonstrates that HPM residue accumulation is associated with impaired seed germination, primarily through metabolic disruption of lipid reserves rather than oxidative damage during germination, highlighting a non-target phytotoxic effect of this herbicide on the crop itself. These findings provide a theoretical basis for understanding the potential toxicity of persistent HPM residues in rapeseed, with implications for pesticide environmental risk assessment and the safe production of rapeseed.