The regulation solutions and mechanisms of reducing pesticide phytotoxicity to nontarget plants are not well-defined and detailed. Here, we have proposed a new detoxification strategy to control the toxic effects of herbicide imazethapyr (IM) induced in wheat seedlings from the perspective of the plasma membrane (PM) H+-ATPase. We found that the changes in PM H+-ATPase activity have a regulatory effect on the phytotoxic effects induced by IM in plants. Treatment with PM H+-ATPase activators restored the reduced auxin content and photosynthetic efficiency caused by IM, thereby promoting plant growth. Application of a PM H+-ATPase inhibitor further reduced phosphorus content and significantly increased 2,4-dihydroxy-7-methoxy-2H,1,4-benzoxazin-3(4H)one (DIMBOA) and jasmonic acid levels. These effects indicate that auxin and DIMBOA may regulate plant growth trends and detoxification effects mediated by PM H+-ATPase. This work opens a new strategy for regulating herbicide toxicity to nontarget plants from the PM H+-ATPase.
Polycyclic aromatic hydrocarbons (PAHs) constitute a category of persistent organic contaminants that possess the potential to induce carcinogenic, teratogenic, and mutagenic consequences. Our previous findings have revealed that plant roots actively take up PAHs through co-transport with protons, and auxin can promote PAHs uptake by wheat roots. It remains unclear whether nitric oxide (NO), a signaling molecule involved in numerous physiological processes in plants and downstream of auxin, can affect PAHs uptake by plant roots. In our study, 50 μmol/L sodium nitroprusside (SNP) significantly enhanced phenanthrene uptake after 4 h of exposure. After the addition of SNP (50 μmol/L), the H + flux on root surface increased, and H + -ATPase activity was activated, indicating that exogenous NO promotes phenanthrene uptake by plant roots via activating H + -ATPase. By studying the effects of 50 μmol/L cyclic guanosine monophosphate (cGMP), 5 mmol/L Ca 2+ , and 50 μmol/L adenosine monophosphate (AMP) on phenanthrene uptake by ryegrass roots and measuring root calcium-dependent protein kinases (CDPK) activity, we demonstrated that exogenous NO promotes phenanthrene uptake through the signaling pathway of NO, cGMP, Ca 2+ , CDPK, 14-3-3 protein and H + -ATPase. The results contribute significant insights into elucidating the underlying mechanisms of NO modulating PAHs absorption by plant roots, thereby offering crucial strategies for advancing food safety measures and enhancing the phytoremediation potential of soils and waters contaminated with PAHs.
As emerging alternatives of legacy perfluoroalkyl substances, perfluorophosphinates (PFPiAs) and perfluorophosphonates (PFPAs) are widely applied in industrial and agricultural fields and are supposed to be large partitioned to soil and highly persistent. It is of particular interest to understand their transfer from roots to shoots and transformation in plants, such as wheat. The results of hydroponic experiments indicated that C6/C6 PFPiA, C8/C8 PFPiA, perfluorooctanophosphonic acid (PFOPA), and perfluorohexaphosphonic acid (PFHxPA) were quickly adsorbed on the epidermis of wheat root (Triticum aestivum L.), which was driven by their hydrophobicity. A small fraction of the accumulated PFPiAs and PFPAs in the wheat root was subjected to absorption via an active process dependent on H+-ATPase. PFHxPA, which has the smallest molecular weight and medium hydrophilicity (log Kow < 4), displayed the strongest absorption efficiency via the water and anion channels and had the highest translocation potential from roots to shoots in wheat. C6/C6 and C8/C8 PFPiAs experienced phase I metabolism in wheat, although at a low rate, to form more persistent PFHxPA and PFOPA, respectively, as well as 1H-perfluorohexane (1H-PFHx) and 1H-perfluorooctane (1H-PFO), which were regulated by cytochrome P450 in wheat root. As a result, exposure to PFPiAs in roots ultimately caused the accumulation of more persistent PFPAs in the above-ground parts of plants, raising concerns on their potential risks on human health.
危险品化学品经营许可证（带存储）