The excessive arsenic (As) accumulation in plant tissues enforced toxic impacts on growth indices. So, the utilization of As-contaminated food leads to risks associated with human health. For the reduction of As concentrations in foods, it is obligatory to fully apprehend the take up, accretion, transportation and toxicity mechanisms of As within plant parts. This metalloid impairs the plant functions by disturbing the metabolic pathways at physio-biochemical, cellular and molecular levels. Though several approaches were utilized to reduce the As-accumulation and toxicity in soil-plant systems. Recently, engineered nanoparticles (ENPs) such a zinc oxide (ZnO), silicon dioxide or silica (SiO₂), iron oxide (FeO) and copper oxide (CuO) have emerged new technology to reduce the As-accumulation or phytotoxicity. But, the mechanistic approaches with systematic explanation are missing. By knowing these facts, our prime focus was to disclose the mechanisms behind the As toxicity and its mitigation by ENPs in higher plants. ENPs relives As toxicity and its oxidative damages by regulating the transporter or defense genes, modifying the cell wall composition, stimulating the antioxidants defense, phytochelatins biosynthesis, nutrients uptake, regulating the metabolic processes, growth improvement, and thus reduction in As-accumulation or toxicity. Yet, As-detoxification by ENPs depends upon the type and dose of ENPs or As, exposure method, plant species and experimental conditions. We have discussed the recent advances and highlight the knowledge or research gaps in earlier studies along with recommendations. This review may help scientific community to develop strategies such as applications of nano-based fertilizers to limit the As-accumulation and toxicity, thus healthy food production. These outcomes may govern sustainable application of ENPs in agriculture.

Iron (III) co-precipitation with dissolved organic matter (DOM) is pervasive in many natural environments. However, the effects of DOM on the formation of Fe(III) hydroxysulfate (FHS) and its environmental implications are poorly understood. In this study, fulvic acid (FA) was used as a model DOM compound, and experiments were devised to investigate the effects of FA on the formation of FHS. In addition, the Pb(II) adsorption capabilities of FHSs biosynthesized under various FA dosages, including kinetics and sorption isotherm experiments, were conducted. These experiments showed that co-precipitation of FA promoted the formation of Fe-FA composites, FA-doped schwertmannite, and small particles of jarosite. Co-precipitates are more enriched in carboxyl (–COOH) functional groups due to their preferential binding with FHS. The adsorption kinetics, isotherms and mechanisms of Pb onto the biosynthesized FHSs were then comprehensively characterized and modeled. Though the specific surface area decreased with increasing FA loading, the introduction of FA into FHSs increased Pb(II) adsorption, with the highest concentration of FA addition improving the removal capacity of Pb(II) to 91.54%. Kinetics studies and intra-particle diffusion models indicated that the adsorption of Pb(II) onto the FHSs was correlated with the number of active sites, and two adsorption steps: surface adsorption and the diffusion of Pb(II) in channels inside the biosynthesized FHSs, are suggested. The adsorption mechanism was attributed to cation exchange between Pb(II) and –OH and –COOH functional groups, and the co-precipitated FA provided additional sites for Pb(II) adsorption by FHS.

Volatile organic compounds (VOCs) promote cyanobacteria dominating eutrophicated waters, with aquatic plant decrease and even disappearance. To uncover the toxic mechanism of cyanobacterial VOCs on aquatic plants, we investigated the growth, photosynthetic pigment levels, photosynthetic abilities and related gene expression in duckweed treated with β-cyclocitral and β-ionone, 2 main components in the VOCs. The levels of chlorophylls and carotenoids gradually declined with raising the concentration of the 2 compounds and prolonging the treatment time. Their decline should result from the down-regulation of 8 genes associated with photosynthetic pigment biosynthesis and up-regulation of 2 genes involved in carotenoid degradation. The reduction was also found in the photosystem II (PSII) efficiency and O₂ evolution rate, which should result from the lowered photosynthetic pigment levels and down-regulation of 38 genes related with photosynthetic process. The frond numbers, total frond area and fresh weight gradually decreased with raising the 2 compound concentration, which may result from the lowered photosynthetic abilities as well as down-regulated expression of 7 genes associated with growth-promoting hormone biosynthesis and signal transduction. It can be speculated that cyanobacterial VOCs may poison aquatic plants by lowering the photosynthesis and growth through altering related gene expression.

Systemic studies on the bioremediation of co-contaminated PAHs and heavy metals are lacking, and this paper provides an in-depth review on the topic. The released sources and transport of co-contaminated PAHs and heavy metals, including their co-occurrence through formation of cation-π interactions and their adsorption in soil are examined. Moreover, it is investigated that co-contamination of PAHs and heavy metals can drive a synergistic positive influence on bioremediation through enhanced secretion of extracellular polymeric substances (EPSs), production of biosynthetic genes, organic acid and enzymatic proliferation. However, PAHs molecular structure, PAHs-heavy metals bioavailability and their interactive cytotoxic effects on microorganisms can exert a challenging influence on the bioremediation under co-contaminated conditions. The fluctuations in bioavailability for microorganisms are associated with soil properties, chemical coordinative interactions, and biological activities under the co-contaminated PAHs-heavy metals conditions. The interactive cytotoxicity caused by the emergence of co-contaminants includes microbial cell disruption, denaturation of DNA and protein structure, and deregulation of antioxidant biological molecules. Finally, this paper presents the emerging strategies to overcome the bioavailability problems and recommends the use of biostimulation and bioaugmentation along with the microbial immobilization for enhanced bioremediation of PAHs-heavy metals co-contaminated sites. Better knowledge of the bioremediation potential is imperative to improve the use of these approaches for the sustainable and cost-effective remediation of PAHs and heavy metals co-contamination in the near future.

Dinotefuran is a third-generation neonicotinoid pesticide and is increasingly used in agricultural production, which has adverse effects on nontarget organisms. However, the research on the impact of dinotefuran on nontarget organisms is still limited. Here the toxic effects of dinotefuran on an important economic species and a model lepidopteran insect, Bombyx mori, were investigated. Exposure to different doses of dinotefuran caused physiological disorders or death. Cytochrome P450, glutathione S-transferase, carboxylesterase, and UDP glycosyl-transferase activities were induced in the fat body at early stages after dinotefuran exposure. By contrast, only glutathione S-transferase activity was increased in the midgut. To overcome the lack of sensitivity of the biological assays at the individual organism level, RNA sequencing was performed to measure differential expressions of mRNA from silkworm larvae after dinotefuran exposure. Differential gene expression profiling revealed that various detoxification enzyme genes were significantly increased after dinotefuran exposure, which was consistent with the upregulation of the detoxifying enzyme. The global transcriptional pattern showed that the physiological responses induced by dinotefuran toxicity involved multiple cellular processes, including energy metabolism, oxidative stress, detoxification, and other fundamental physiological processes. Many metabolism processes, such as carbon metabolism, fatty acid biosynthesis, pyruvate metabolism, and the citrate cycle, were partially repressed in the midgut or fat body. Furthermore, dinotefuran significantly activated the MAPK/CREB, CncC/Keap1, PI3K/Akt, and Toll/IMD pathways. The links between physiological, biochemical toxicity and comparative transcriptomic analysis facilitated the systematic understanding of the integrated biological toxicity of dinotefuran. This study provides a holistic view of the toxicity and detoxification metabolism of dinotefuran in silkworm and other organisms.

Bensulfuron-methyl (BSM) residues in soil threaten the rotation of BSM-sensitive crops. Microbial biofilms formed on crop roots could improve the ability of microbes to survive and protect crop roots. However, the research on biofilms with the purpose of mitigating or even eliminating BSM damage to sensitive crops is very limited. In this study, one BSM-degrading bacterium, Hansschlegelia zhihuaiae S113, colonized maize roots by forming a biofilm. Root exudates were associated with increased BSM degradation efficiency with strain S113 in rhizosphere soil relative to bulk soil, so the interactions among BSM degradation, root exudates, and biofilms may provide a new approach for the BSM-contaminated soil bioremediation. Root exudates and their constituent organic acids, including fumaric acid, tartaric acid, and l-malic acid, enhanced biofilm formation with 13.0–22.2% increases, owing to the regulation of genes encoding proteins responsible for cell motility/chemotaxis (fla/che cluster) and materials metabolism, thus promoting S113 population increases. Additionally, root exudates were also able to induce exopolysaccharide production to promote mature biofilm formation. Complete BSM degradation and healthy maize growth were found in BSM-contaminated rhizosphere soil treated with wild strain S113, compared to that treated with loss-of-function mutants ΔcheA-S113 (89.3%, without biofilm formation ability) and ΔsulE-S113 (22.1%, without degradation ability) or sterile water (10.7%, control). Furthermore, the biofilm mediated by organic acids, such as l-malic acid, exhibited a more favorable effect on BSM degradation and maize growth. These results showed that root exudates and their components (such as organic acids) can induce the biosynthesis of the biofilm to promote BSM degradation, emphasizing the contribution of root biofilm in reducing BSM damage to maize.

Understanding the metabolic defense and compensation to maintain homeostasis is crucial for assessing the potential health risk of organic pollutants in crops. Currently, limited understanding is available regarding the targeted metabolic pathways and response mechanism under contaminant stress. This study showed that ciprofloxacin (CIP) at the environmental concentrations (1, 5, 25, 50 mg/L) did not significantly inhibit growth or cause severe oxidative damage to rice (Oryza sativa L.). Instead, the increment in CIP concentration induced a series of sequential metabolic disorders, which were characterized predominantly by primary and secondary metabolic disturbances, including phenylpropanoid biosynthesis, the carbohydrate, lipid and amino acid metabolism. After CIP in vivo exceeded a certain threshold level (>0.29 mg/g dry weight), β-glucosidases (BGLUs) mediated the transition from the activation of the genes related to phenylpropanoid biosynthesis to the inhibition of the genes related to carbohydrate metabolism in rice. In particular, starch and sucrose metabolism showed the most profound perturbation stressed by environmental concentrations of CIP (5 mg/L) and other tested organic pollutants (10 μg/L of tricyclazole, thiamethoxam, polybrominated diphenyl ethers, and polychlorinated biphenyls). Besides, the key genes encoding endoglucanase and BGLU were significantly downregulated (|log₂FC| > 3.0) under 100 μg/L of other tested organic pollutants, supporting the transition from the activation of secondary defense metabolism to the disruption of primary energy metabolism. Thus, in addition to bioaccumulation, changes in BGLU activity and starch and sucrose metabolism can reflect the potential adverse effects of pollutants on rice. This study explained the stepwise metabolic and transcriptional responses of rice to organic pollutants, which provided a new reference for the comprehensive evaluation of their environmental risks.

Carbendazim (CBZ), a broad-spectrum pesticide frequently detected in fruits and vegetables, could trigger potential toxic risks to mammals. To facilitate the assessment of health risks, this study aimed to characterize the cytochrome P450 (CYPs)-mediated metabolism profiles of CBZ by a combined experimental and computational study. Our results demonstrated that CYPs-mediated region-selective hydroxylation was a major metabolism pathway for CBZ in liver microsomes from various species including rat, mouse, minipig, dog, rabbit, guinea pig, monkey, cow and human, and the metabolite was biosynthesized and well-characterized as 6-OH-CBZ. CYP1A displayed a predominant role in the region-selective hydroxylation of CBZ that could attenuate its toxicity through converting it into a less toxic metabolite. Meanwhile, five other common pesticides including chlorpyrifos-methyl, prochloraz, chlorfenapyr, chlorpyrifos, and chlorothalonil could significantly inhibit the region-selective hydroxylation of CBZ, and consequently remarkably increased CBZ exposure in vivo. Furthermore, computational study clarified the important contribution of the key amino acid residues Ser122, and Asp313 in CYP1A1, as well as Asp320 in CYP1A2 to the hydroxylation of CBZ through hydrogen bonds. These results would provide some useful information for the metabolic profiles of CBZ by mammalian CYPs, and shed new insights into CYP1A-mediated metabolic detoxification of CBZ and its health risk assessment.

Insufficient evidence exists regarding the visible physiological toxic endpoints of MPs exposures on zebrafish larvae due to their small sizes. Herein, the impacts of micro-polystyrene particles (μ-PS) and 100 nm polystyrene particles (n-PS) on the toxicity of cadmium (Cd) through altering neutrophil expressions were identified and quantified in the transgenic zebrafish (Danio rerio) larvae Tg(lyz:DsRed2), and the effects were size-dependent. When exposed together with μ-PS, the amount of neutrophils in Cd treated zebrafish larvae decreased by 25.56% through reducing Cd content in the larvae. By contrast, although n-PS exposure caused lower Cd content in the larvae, the expression of neutrophils under their combined exposure remained high. The mechanism of immune toxicity was analyzed based on the results of metabonomics. n-PS induced high oxidative stress in the larvae, which promoted taurine metabolism and unsaturated fatty biosynthesis in n-PS + Cd treatment. This observation was accordance with the significant inhibition of the activities of superoxide dismutase and catalase enzymes detected in their combined treatment. Moreover, n-PS promoted the metabolic pathways of catabolic processes, amino acid metabolism, purine metabolism, and steroid hormone biosynthesis in Cd treated zebrafish larvae. Nanoplasctis widely coexist with other pollutants in the environment at relatively low concentrations. We conclude that more bio-markers of immune impact should be explored to identify their toxicological mechanisms and mitigate the effects on the environment.

A paradoxical impact of high rates of production and consumption of antibiotics is their widespread release in the environment. Consequently, low concentrations of antibiotics and their byproducts have been routinely identified from various environmental settings especially from aquatic environments. However, the impact of such low concentrations of antibiotics on the exposed host especially in early life remains poorly understood. We exposed zebrafish to two different environmental concentrations of oxytetracycline and sulfamethoxazole, from larval stage to adulthood (∼120 days) and characterized their impact on the taxonomic diversity, antibiotic resistance genes, and metabolic pathways of the gut microbiome using metagenomic shotgun sequencing and analysis. Long term exposure of environmental concentrations of oxytetracycline and sulfamethoxazole significantly impacted the taxonomic composition and metabolic pathways of zebrafish gut microbiome. The antibiotic exposed samples exhibited significant enrichment of multiple flavobacterial species, including Flavobacterium sp. F52, Flavobacterium johnsoniae and Flavobacterium sp. Fl, which are well known pathogenic bacteria. The relative abundance of antibiotic resistance genes, especially several tetratcycline and sulfonamide resistance genes were significantly higher in the exposed samples and showed a linear correlation with the antibiotic concentrations. Furthermore, several metabolic pathways, including folate biosynthesis, oxidative phosphorylation, and biotin metabolism pathways, showed significant enrichment in the antibiotic exposed samples. Collectively, our results suggest that early life exposure of the environmental concentrations of antibiotics can increase the abundance of unfavorable bacteria, antibiotic resistance genes and associated pathways in the gut microbiome of zebrafish.