Li_2025_Environ.Int_204_109809

Phoxim, an organophosphorus insecticide (OP), poses risks to non-target organisms in the environment. However, the biodegradation mechanism of phoxim was not fully understood. In this study, a novel detoxification pathway for phoxim in Delftia lacustris PX-1 was identified. A gene cluster pho (phoABC1C2DEFGHI), located on the plasmid, was found to be involved in phoxim degradation. The genes phoA, phoB, and phoD, which were responsible for converting phoxim to benzoate, were functionally characterized in vitro. Notably, PhoA was highly abundant in global cultivated lands. Moreover, acute toxicity experiments showed that both phoxim and its metabolite, 2-hydroxyimino-2-phenylacetonitrile (2H2P), exhibited moderate toxicity to zebrafish, whereas strain PX-1 could detoxify both compounds through degradation. After exposure to 2 mg L(-1) phoxim, the brain acetylcholinesterase (AChE) activity levels of zebrafish dramatically decreased by 31.28 % (P < 0.05) relative to unexposed controls. Interestingly, phoxim could promote the colonization of strain PX-1 in the zebrafish gut, which mitigated phoxim-induced damage to AChE activity in the zebrafish brain. In summary, our research reveals a novel phoxim detoxification mechanism and provides a theoretical foundation for the bioremediation of residual phoxim in the environment. IN BRIEF: This study reveals a novel metabolic pathway for phoxim biodegradation and elucidates the detoxification mechanism of strain PX-1 in zebrafish.