The widespread use of herbicides poses escalating threats to ecosystem stability and food safety, underscoring the urgent need to elucidate plant-based detoxification mechanisms. However, the contrasting roles of secondary metabolites like DIMBOA and flavonoids in mitigating herbicide toxicity in wheat remain unclear. Research indicates that DIMBOA primarily acts as a defense metabolite, reducing reactive oxygen species (ROS) accumulation through iron chelation and reinforcing structural defenses, but its growth recovery is limited due to metabolic competition with auxin biosynthesis. In contrast, flavonoids exhibit a "triple protection mechanism," simultaneously maintaining antioxidant defense, improving iron homeostasis, and preserving tryptophan synthase activity, thereby restoring auxin and lignin biosynthesis and achieving coordinated detoxification and growth recovery. As a common precursor, shikimic acid further amplifies these protective effects. To summarize, DIMBOA and flavonoids mitigate oxidative stress, maintain iron balance, and reduce herbicide residues in wheat through distinct regulatory pathways. The findings provide valuable insights into secondary metabolite regulation and offer potential strategies for sustainable herbicide detoxification in agricultural ecosystems.

Antimony (Sb) treatment presents a paradox: oxidizing toxic Sb(III) to Sb(V) for detoxification generates Sb(OH)(6)(-) species with a large hydration radius (7.36 & Aring;) that hinders adsorption on conventional crystalline adsorbents due to limited accessible sites. We developed a Ce(III/IV)-chitosan semi-crystalline complex with mixed-valence coordination (Ce3+/Ce4+ = 62.3:37.7) that addresses this challenge. Ce coordination constructs a semi-crystalline architecture where amorphous regions provide more accessible sites for large Sb(OH)(6)(-) while ordered domains maintain structural stability. The mixed-valence system sustained positive surface charge (+25 to +40 mV, pH 2-10) for electrostatic Sb(V) attraction, while Ce3+/Ce4+ cycling catalyzed H2O2-mediated Sb(III) oxidation. At 2 mg/L Sb, a challenging concentration for industrial wastewater, the material achieved >98% removal within 90 min, reducing residual Sb to <0.04 mg/L. Maximum capacities reached 595.5 mg/g (Sb(V)) and 461.6 mg/g (Sb(III)), with excellent regenerability (>86% after five cycles). This work demonstrates how coordination-induced structural reorganization and mixed-valence chemistry overcome fundamental barriers in mixed-oxidation-state contaminant treatment.

Tetracycline (TC) antibiotics are common trace pollutants in aquatic environments, where they can accumulate and transform into epimers such as 4-epi-tetracycline (ETC), potentially increasing ecotoxicity. Therefore, developing effective and safe in-situ remediation technologies for the removal of TCs from natural waters is of critical importance. This study presents a fabrication method for magnetic chitosan-supported mixed-phase FeOOH particles (alpha/6-FeOOH@CS), which are enriched with oxygen vacancies, for the adsorption and degradation of TCs. Significant epimerization of TC into ETC was observed during its removal. Batch experiments showed that 96% of TC and 97.6% of ETC could be removed by alpha/6-FeOOH@CS. The main mechanism involves the chitosan-induced accumulation, Fe(III)-mediated complexation and oxidation, coupled with reactive oxygen species (ROS) generation initiated by Fe(II). These processes establish a self-sustaining Fe(III)/Fe(II) redox cycle for efficient in-situ remediation of TCs. The differing removal behaviors of TC and ETC are likely attributed to their distinct interactions with Fe(III), resulting from spatial changes in the C4 dimethylamino group. Additionally, algal toxicity tests conducted throughout the degradation process confirmed the near non-toxic nature of the removal steps, indicating that no significant new environmental toxic effects were introduced.

Herbicide residues in agroecosystems pose ecological and food safety risks, yet sustainable mitigation strategies that reduce chemical inputs while enhancing in situ detoxification remain scarce. Here, we developed a pH-responsive, bio-based indole-chitosan microparticle system designed to activate plasma membrane H+-ATPase in plants, thereby accelerating herbicide metabolism and minimizing herbicide residues in crops to enhance food safety. Under simulated rhizosphere conditions (pH 5.5), the microparticles achieved controlled indole release, increasing in-plant bioavailability by 35 % compared to direct indole application. Using wheat and imazethapyr as a model, the system reduced herbicide residues by 46 % and active ingredient use by 40 %, while avoiding additional environmental risks. This mechanism-driven approach enhances both Phase I and Phase II detoxification pathways, restores iron homeostasis, and coordinates growth-defense responses, offering a scalable and environmentally benign solution for mitigating residual agrochemical burdens. By integrating toxicological assessment with active detoxification regulation, this study bridges environmental toxicology and toxicity regulation, providing a transferable, mechanism-guided strategy for sustainable agrochemical risk mitigation.

Amid increasing concerns over fluorinated compounds, the Organization for Economic Co-operation and Development (OECD) has reclassified numerous fluorinated pesticides as per- and polyfluoroalkyl substances (PFAS), yet their metabolite distribution in plants remains unexplored. Using flufenacet as a model compound, this study investigated the metabolic distribution in wheat. We discovered a "reverse distribution" phenomenon where the parent compound mainly concentrated in roots (translocation factor = 0.08), while metabolites preferentially accumulated in shoots. The three metabolites with the highest shoot responses, M07, M10, and M15, showed TF values of 1.54, 2.37, and 1.67, respectively. This pattern challenges traditional lipophilicity-based transport theories and increases food chain exposure risks. Toxicity assessment revealed that despite lower acute toxicity, these metabolites exhibited higher hepatotoxicity, mutagenicity, and carcinogenicity than the parent compound, with M10 showing higher carcinogenic potential. Molecular docking demonstrated binding to human proteins with energies of -6.01 to -7.34 kcal/mol. Findings suggest revising risk assessment frameworks to incorporate metabolite distribution and toxicological properties for PFAS pesticide management.

Non-target plants play a key role in maintaining ecological balance and biodiversity. Here, we studied the effect of the chiral herbicide imazethapyr (IM) on the flowering initiation of the non-target plant Arabidopsis thaliana and its underlying mechanism. Plants treated with R-IM initiated flowering earlier than those treated with S-IM. The herbicidally active R-IM had a much greater effect on various phytohormones than S-IM, and this effect increased with the concentration of R-IM. Before flowering, R-IM had a significant effect on the internal levels of 1-aminocyclopropane-1-carboxylic acid (ACC), indole-3-acetic acid (IAA), abscisic acid (ABA), and gibberellic acid (GA3) in Arabidopsis plants, which indicated that it promoted the production of ACC, and high concentrations of R-IM also promoted IAA, ABA, and GA3. R-IM promoted ACC, IAA, and GA3 before and during flowering. High concentrations of R-IM strongly promoted IAA and inhibited GA3, and R-IM inhibited or promoted ACC depending on the concentrations applied. Thus, earlier flowering of Arabidopsis under R-IM treatment may be affected by phytohormone levels throughout the plant, and IAA, ACC, and GA3 likely have significant effects on flowering.

The plasma membrane (PM) H+-ATPase is crucial for a plant defense system. However, there is currently no consensus on whether the PM H+-ATPase plays a role in alleviating the toxic effects of herbicides on nontarget plants. We found that under the herbicide imazethapyr (IM) exposure, PM H+-ATPase activity in wheat roots increased by approximately 69.53%, leading to rhizosphere acidification. When PM H+-ATPase activity is inhibited, the toxicity of IM significantly increases: When exposed to IM alone, the total Fe content of wheat roots decreased by 29.07%, the relative Fe2+ content increased by 27.75%, and the ROS content increased by 27.74%. When the PM H+-ATPase activity was inhibited, the corresponding data under IM exposure were 37.36%, 215%, and 57.68%, respectively. This work delves into the role of PM H+-ATPase in mediating the detoxification mechanism in plants exposed to herbicides, offering new insights into enhancing crop resistance against herbicides.

Controlling and mitigating the toxicity of herbicides to non-target plants is of significant importance in reducing ecological risks. The development of green and natural herbicide control technologies has become an urgent necessity. In this paper, how 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazine-3(4H)-one (DIMBOA) and baicalein alleviated oxidative stress induced by imazethapyr (IM) in wheat seedlings was investigated. We found that DIMBOA and baicalein enhanced the antioxidant enzyme activities in wheat seedlings exposed to IM and reduced the excessive reactive oxygen species due to IM stress by 21.3

Herbicides are known to affect the soil nitrogen cycle by shaping soil microorganisms. However, it is not clear how herbicides regulate diverse transformation processes of soil nitrogen cycling by altering rhizosphere microorganisms, subsequently influencing the feedback to plant nitrogen metabolism. Here, we investigated how imazethapyr (IM) enantiomers drive plant-soil feedback on nitrogen metabolism by altering the rhizosphere microorganisms. The results indicated that ( R )- and ( S )-IM significantly changed the composition and structure rhizosphere microbiome with enantioselectivity and functional changes in microbial communities were associated with soil nitrogen circulation. The determination of nitrogen-cycling functional genes further supported the above findings. The results revealed that ( R )- and ( S )-IM could change the abundance of nitrogen-cycling functional genes by changing specific bacteria abundances, such as Bacteroidetes, Proteobacteria, and Acidobacteria, thus resulting in diverse nitrogen transformation processes. The alternation of nitrogen transformation processes indicated ( R )-IM exhibited a more notable tendency to form a nitrogen cycling pattern with lower energy cost and higher nitrogen retention than ( S )-IM. Sterilization experiments demonstrated changes in soil nitrogen cycling drive plant nitrogen metabolism and rhizosphere microorganisms are responsible for the above process of plant-soil feedback for nitrogen metabolism. Under IM enantiomer treatments, rhizosphere microorganisms might stimulate glutamate synthesis by promoting NH 4 + uptake and glutamine-glutamate synthesis cycling in roots, thus contributing to positive feedback, with ( R )-IM treatments showing more pronounced positive feedback on nitrogen metabolism than ( S )-IM treatments. Our results provide theoretical support for determining the mechanism by which IM enantiomers drive plant-soil nitrogen metabolism by changing the rhizosphere microbial communities.

As representatives of allelopathy, weeds consistently coexist with crops, exhibiting mutual growth inhibition. At the same time, herbicides are usually employed to control weeds. However, few studies have investigated how herbicides will affect allelopathy between crops and their neighboring weeds. Our findings suggested that allelopathic-induced phenotypic variations in ryegrass were reduced in the presence of the herbicide imazethapyr (IM), consistent with the antioxidant system analysis results. Additionally, IM affected the levels of allelochemical hydroxamic acid (Hx) in both plants. Hydroponic experiments revealed that this impact was due to the accelerated transportation of Hx from wheat to ryegrass, driven by ryegrass-secreted jasmonic acid. This study holds paramount significance for comprehending the effects of herbicides on the allelopathic interactions between nontargeted crops and neighboring weeds, contributing to an enhanced understanding of herbicides on plant species interactions.

Plant fatty acids (FAs) are critical components of lipids and play an important role in coping with pollution-induced stress. However, the relationship between the fluctuating changes of FAs and the toxic effects of pollutants is not clear. Here, we analyzed and identified 19 FAs, namely 14 medium and long chain fatty acids (MLCFAs) and 5 very long chain fatty acids (VLCFAs). First, a positive correlation between plant biomass and LCFA content was observed. Changes in unsaturation were inversely related to cell membrane permeability, which serves as an indicator of the toxic effects. In particular, the use of herbicides led to a reduction in total FA content, but caused a significant increase in free fatty acids (FFAs), which facilitate oxidative stress. In addition, supplementation with exogenous FAs, particularly linoleic and alpha-linolenic acids, effectively alleviated the toxic inhibition. (R)-dichlorprop causes abnormal FA metabolism that can be reversed by ferrostatin-1, a ferroptosis inhibitor. Under (R)-dichlorprop exposure, the balance of FA unsaturation in plants is disrupted by inhibition of FA desaturase activity, ultimately leading to ferroptosis and disruption of cell membrane integrity. This study aims to enhance the understanding of the ecotoxic effects of herbicides by examining changes in FAs. The findings will provide a scientific basis for controlling environmental risks associated with hazardous substances.

The effects of co-exposure to antibiotics and microplastics in agricultural systems are still unclear. This study investigated the effects of florfenicol (FF) and polystyrene microplastics (PS-MPs) on photosynthetic carbon assimilation in rice seedlings. Both FF and PS-MPs inhibited photosynthesis, while PS-MPs can alleviate the toxicity of FF. Chlorophyll synthesis genes (HEMA, HEMG, CHLD, CHLG, CHLM, and CAO) were down-regulated, whereas electron transport chain genes (PGR5, PGRL1A, PGRL1B, petH, and ndhH) were up-regulated. FF inhibited linear electron transfer (LET) and activated cyclic electron transfer (CET), which was consistent with the results of the chlorophyll fluorescence parameters. The photosynthetic carbon assimilation pathway was altered, the C3 pathway enzyme Ribulose1,5-bisphosphatecarboxylase/oxygenase (RuBisCO) was affected, C4 enzyme ((phosphoenolpyruvate carboxykinase (PEPCK), pyruvate orthophosphate dikinase (PPDK), malate dehydrogenase (MDH), and phosphoenolpyruvate carboxylase (PEPC))) and related genes were significantly up-regulated, suggesting that the C3 pathway is converted to C4 pathway for self-protection. The key enzymes involved in photorespiration, glycolate oxidase (GO) and catalase (CAT), responded positively, photosynthetic phosphorylation was inhibited, and ATP content and H+-ATPase activity were suppressed, nutrient content (K, P, N, Ca, Mg, Fe, Cu, Zn, Mn, and Ni) significantly affected. Transcriptomic analysis showed that FF and PS-MPs severely affected the photosynthetic capacity of rice seedlings, including photosystem I, photosystem II, non-photochemical quenching coefficients, and photosynthetic electron transport.

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.

Effectively controlling target organisms while reducing the adverse effects of pesticides on non-target organisms is a crucial scientific inquiry and challenge in pesticide ecotoxicology research. Here, we studied the alleviation of herbicide (R)-imazethapyr [(R)-IM] to non-target plant wheat by active regulation between auxin and secondary metabolite 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazine-3(4H)-one (DIMBOA). We found (R)-IM reduced 32.4% auxin content in wheat leaves and induced 40.7% DIMBOA accumulation compared to the control group, which effortlessly disrupted the balance between wheat growth and defense. Transcriptomic results indicated that restoration of the auxin level in plants promoted the up-regulation of growth-related genes and the accumulation of DIMBOA up-regulated the expression of defense-related genes. Auxin and DIMBOA alleviated herbicide stress primarily through effects in the two directions of wheat growth and defense, respectively. Additionally, as a common precursor of auxin and DIMBOA, indole adopted a combined growth and defense strategy in response to (R)-IM toxicity, i.e., restoring growth development and enhancing the defense system. Future regulation of auxin and DIMBOA levels in plants may be possible through appropriate methods, thus regulating the plant growth-defense balance under herbicide stress. Our insight into the interference mechanism of herbicides to the plant growth-defense system will facilitate the design of improved strategies for herbicide detoxification.

Antibiotics and microplastics (MPs) are two emerging pollutants in agroecosystems, however the effects of coexposure to antibiotics and MPs remain unclear. The toxicity of florfenicol (FF) and polystyrene microplastics (PS-MPs) on rice seedlings was investigated. FF and PS-MPs caused colloidal agglomeration, which changed the environmental behavior of FF. FF inhibited rice growth and altered antioxidant enzyme (superoxide dismutase, peroxidase, and catalase) activities, leading to membrane lipid peroxidation; impaired photosynthetic systems, decreased photosynthetic pigments (Chlorophyll a, Chlorophyll b, and carotene), chlorophyll precursors (Proto IX, Mg-Proto IX, and Pchlide), photosynthetic and respiratory rates. The key photosynthesis related genes (PsaA, PsaB, PsbA, PsbB, PsbC, and PsbD) were significantly down-regulated. The ultrastructure of mesophyll cells was destroyed with chloroplast swelling, membrane surface blurring, irregular thylakoid lamellar structure, and number of peroxisomes increased. PS-MPs mitigated FF toxicity, and the IBR index values showed that 10 mg & BULL;L-1 PS-MPs were more effective. Metabolomic analysis revealed that the abundance of metabolites and metabolic pathways were altered by FF, was greater than the combined "MPs-FF" contamination. The metabolism of amino acids, sugars, and organic acids were severely interfered. Among these, 15 metabolic pathways were significantly altered, with the most significant effects on phenylalanine metabolism and the citric acid cycle (p < 0.05).

The ecological effects of quinolone antibiotics (QNs) on non-target organisms have received widespread attention. The toxicological mechanisms of three common QNs, that is, enrofloxacin, levofloxacin, and ciprofloxacin, on soybean seedlings were investigated in this study. Enrofloxacin and levofloxacin caused significant growth inhibition, ultrastructural alterations, photosynthetic suppression, and stimulation of the antioxidant system, with levofloxacin exhibiting the strongest toxic effects. Ciprofloxacin (<1 mg·L-1) did not have a significant effect on the soybean seedlings. As the concentrations of enrofloxacin and levofloxacin increased, antioxidant enzyme activities, malondialdehyde content, and hydrogen peroxide levels also increased. Meanwhile, the chlorophyll content and chlorophyll fluorescence parameters decreased, indicating that the plants underwent oxidative stress and photosynthesis was suppressed. The cellular ultrastructure was also disrupted, which was manifested by swollen chloroplasts, increased starch granules, disintegration of plastoglobules, and mitochondrial degradation. The molecular docking results suggested that the QNs have an affinity for soybean target protein receptors (4TOP, 2IUJ, and 1FHF), with levofloxacin having the highest binding energy (-4.97, -3.08, -3.8, respectively). Transcriptomic analysis has shown that genes were upregulated under the enrofloxacin and levofloxacin treatments were mainly involved in ribosome metabolism and processes to synthesize oxidative stress-related proteins. Downregulated genes in the levofloxacin treatment were primarily enriched in photosynthesis-related pathways, indicating that levofloxacin significantly inhibited gene expression for photosynthesis. Genes expression level by quantitative real-time PCR analysis was consistent with the transcriptomic results. This study confirmed the toxic effect of QNs on soybean seedlings, and provided new insights into the environmental risks of antibiotics.

The removal of Cr(VI) from wastewater still faces many challenges. This study reports on chitosan-induced synthesis of few-layer MoS2/Fe-doped biochar (Mo-Fe0.5-CS) with dual applications in Cr(VI) removal. Using chitosan as a soft template, the MoS2 in the composite had only about 3 layers with an interlayer spacing greater than that of pure MoS2, while Fe was embedded in the carbon skeleton in the form of 6-coordination with O/N. The Mo-Fe0.5-CS composite showed high affinity for Cr(VI), with rapid adsorption reaching 100% removal within 15 min for a single solution of Cr(VI). It follows the Langmuir isotherm model with a maximum adsorption capacity of up to 180 mg/g. Furthermore, the Mo-Fe0.5-CS composite demonstrated catalytic activity for Fenton-like reactions, which allowed for the simultaneous removal of organic pollutants and Cr(VI). In a mixture solution of Cr(VI) and Acid Red 73 (AR73), the removal efficiencies using Mo-Fe0.5-CS and H2O2 in 30 min were 99.7% and 96.6%, respectively. The MoS2 acted as a cocatalyst to improve the reduction of Fe(III), and the catalysis of Cr(VI) also contributed to the removal of AR73 to a certain extent. Even at pH 10, the system was effective due to the 1O2 produced in the reaction and the acidic microenvironment constructed by unsaturated S atoms. These findings provide insights into the effective removal and utilization of Cr(VI) in wastewater treatment.

The Fe(III)/Fe(II) redox cycle is the main factor limiting the effectiveness of Fe-mediated advanced oxidation processes (AOPs) for the degradation of organic pollutants. In this study, the promoting effects of thin-layer Al2O3 (t-Al2O3) between the frequently used FeCu components and the mesoporous silica support were studied to reduce Fe(III) to promote the activity of the Fenton-like catalyst. After modification by t-Al2O3, the mesoporous silicon-loaded FeCu catalyst removed 97% of Rhodamine B at pH 7, which was superior to the unmodified sample with a removal rate of 62.4% under the same conditions. Morphological characterization and X-ray diffraction patterns indicated that the Fe-Cu/t-Al2O3 active components were highly dispersed. Pyridine infrared spectra suggested that all of the acid sites were Lewis acids, and the t-Al2O3-loaded samples provided moderate/strong Lewis acids. The loading of t-Al2O3 between the FeCu complex and mesoporous silica support facilitated electron transfer during the Fe(III)/Fe(II) redox cycle by enhancing the dispersion of Fe-Cu/t-Al2O3 and the Lewis acidity. The results of this study provide insight into how t-Al2O3 promoted the interactions between the active components and silica support and how it can be used to aid in the selection of suitable wastewater treatment technologies.

The responses of trace elements and secondary metabolites to stress can reflect plant adaptation to the environment. If and how the imperative trace element Fe and the defensive secondary metabolite 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazine-3(4H)-one (DIMBOA) mediate the toxicity of chiral herbicides to nontarget plants remains inconclusive. We found that the herbicidal-active imazethapyr enantiomer [(R)-IM] stimulated heme oxygenase-1 activity, triggered the release of the catalytic product Fe2+, increased reactive oxygen species production, decreased the DIMBOA content, and increased the DIMBOA-Fe content. XAFS analyses and in vitro Fenton assays demonstrated that DIMBOA could relieve phytotoxicity by chelating excessive Fe3+ to restore Fe homeostasis. The free radical scavenging ability of the chelate of DIMBOA and Fe was also involved. This work refines the dual role of DIMBOA and Fe in mediating the enantioselective phytotoxicity of chiral herbicides, which provides a new direction for improving the herbicide resistance of crops.