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.

Plants detoxify toxic metal(loid)s by accumulating diverse metabolites. Beside scavenging excess reactive oxygen species (ROS) induced by metal(loid)s, some metabolites chelate metal(loid) ions. Classically, thiol-containing compounds, especially glutathione (GSH) and phytochelatins (PCs) are thought to be the major chelators that conjugate with metal(loid)s in the cytoplasm followed by transport and sequestration in the vacuole. In addition to this classical detoxification pathway, a role for secondary metabolites in metal(loid) detoxification has recently emerged. In particular, anthocyanins, a kind of flavonoids with ROS scavenging potential, contribute to enhanced arsenic tolerance in several plant species. Evidence is accumulating that, in analogy to GSH and PCs, anthocyanins may conjugate with arsenic followed by vacuolar sequestration in the detoxification event. Exogenous application or endogenous accumulation of anthocyanins enhances arsenic tolerance, leading to improved plant growth and productivity. The application of some plant hormones and signaling molecules stimulates endogenous anthocyanin synthesis which confers tolerance to arsenic stress. Anthocyanin biosynthesis is transcriptionally regulated by several transcription factors, including myeloblastosis (MYBs). The light-regulated transcription factor elongated hypocotyl 5 (HY5) also affects anthocyanin biosynthesis, but its role in arsenic tolerance remains elusive. Here, we review the mechanism of arsenic detoxification in plants and the potential role of anthocyanins in arsenic tolerance beyond the classical points of view. Our analysis proposes that anthocyanin manipulation in crop plants may ensure sustainable crop yield and food safety in the marginal lands prone to arsenic pollution.

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.

Ethylene regulates plant root growth and resistance to environment stress. However, the role and mechanism of ethylene signaling in response to Cd stress in rice remains unclear. Here, we revealed that ethylene signaling plays a positive role in the resistance of rice to Cd toxicity. Blocking the ethylene signal facilitated root elongation under normal conditions, but resulted in severe oxidative damage and inhibition of root growth under Cd stress. Conversely, ethylene signal enhancement by EIN2 overexpression caused root bending, similar to the response of roots to Cd stress, and displayed higher Cd tolerance than the wildtype (WT) plants. Comparative transcriptome analysis indicated EIN2-mediated upregulation of genes involved in flavonoid biosynthesis and peroxidase activity under Cd stress. The synthesis of phenolic acids and flavonoids were positively regulated by ethylene. Thus, the ein2 (ethylene insensitive 2) mutants displayed lower ROS scavenging capacity than the WT. Moreover, a significant increase in Cd accumulation and relatively increased apoplastic flow were observed in the root apex of the ein2 mutant compared with the WT plants. Overall, EIN2-mediated Cd resistance in rice is mediated by the upregulation of flavonoid biosynthesis and peroxidase activity to induce ROS scavenging, and apoplastic transport barrier formation reduces Cd uptake.

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.

Bacteria play crucial roles in the biogeochemical cycle of arsenic (As) and selenium (Se) as these elements are metabolized via detoxification, energy generation (anaerobic respiration) and biosynthesis (e.g. selenocysteine) strategies. To date, arsenic and selenium biomineralization in bacteria were studied separately. In this study, the anaerobic metabolism of As and Se in Shewanella sp. O23S was investigated separately and mixed, with an emphasis put on the biomineralization products of this process. Multiple analytical techniques including ICP-MS, TEM-EDS, XRD, Micro-Raman, spectrophotometry and surface charge (zeta potential) were employed. Shewanella sp. O23S is capable of reducing selenate (SeO₄²⁻) and selenite (SeO₃²⁻) to red Se(-S)⁰, and arsenate (AsO₄³⁻) to arsenite (AsO₃³⁻). The release of H₂S from cysteine led to the precipitation of AsS minerals: nanorod AsS and granular As₂S₃. When As and Se oxyanions were mixed, both As–S and Se(-S)⁰ biominerals were synthesized. All biominerals were extracellular, amorphous and presented a negative surface charge (−24 to −38 mV). Kinetic analysis indicated the following reduction yields: SeO₃²⁻ (90%), AsO₄³⁻ (60%), and SeO₄²⁻ (<10%). The mix of SeO₃²⁻ with AsO₄³⁻ led to a decrease in As removal to 30%, while Se reduction yield was unaffected (88%). Interestingly, SeO₄²⁻ incubated with AsO₄³⁻ boosted the Se removal (71%). The exclusive extracellular formation of As and Se biominerals might indicate an extracellular respiratory process characteristic of various Shewanella species and strains. This is the first study documenting a complex interplay between As and Se oxyanions: selenite decreased arsenate reduction, whereas arsenate stimulated selenate reduction. Further investigation needs to clarify whether Shewanella sp. O23S employs multi-substrate respiratory enzymes or separate, high affinity enzymes for As and Se oxyanion respiration.

Lead is a metal that exists naturally in the Earth's crust and is a ubiquitous environmental contaminant. The alleviation of lead toxicity is important to keep human health under lead exposure. Biosynthesized selenium nanoparticle (SeNPs) and selenium-enriched Lactobacillus rhamnosus SHA113 (Se-LRS) were developed in this study, and their potentials in alleviating lead-induced injury to the liver and intestinal tract were evaluated in mice by oral administration for 4 weeks. As results, oral intake of lead acetate (150 mg/kg body weight per day) caused more than 50 times and 100 times lead accumulation in blood and the liver, respectively. Liver function was seriously damaged by the lead exposure, which is indicated as the significantly increased lipid accumulation in the liver, enhanced markers of liver function injury in serum, and occurrence of oxidative stress in liver tissues. Serious injury in intestinal tract was also found under lead exposure, as shown by the decrease of intestinal microbiota diversity and occurrence of oxidative stress. Except the lead content in blood and the liver were lowered by 52% and 58%, respectively, oral administration of Se-LRS protected all the other lead-induced injury markers to the normal level. By the comparison with the effects of normal L. rhamnosus SHA113 and the SeNPs isolated from Se-LRS, high protective effects of Se-LRS can be explained as the extremely high efficiency to promote lead excretion via feces by forming insoluble mixture. These findings illustrate the developed selenium-enriched L. rhamnosus can efficiently protect the liver and intestinal tract from injury by lead.

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.

Perfluorooctane sulfonate (PFOS) is associated with male reproductive disorder, but the related mechanisms are still unclear. In this study, we used in vivo and in vitro models to explore the role of Sertoli cell-derived exosomes (SC-Exo)/miR-9-3p/StAR signaling pathway on PFOS-induced suppression of testosterone biosynthesis. Forty male ICR mice were orally administrated PFOS (0.5–10 mg/kg/bw) for 4 weeks. Bodyweight, organ index, sperm count, reproductive hormones were evaluated. Primary Sertoli cells and Leydig cells were used to delineate the molecular mechanisms that mediate the effects of PFOS on testosterone biosynthesis. Our results demonstrated that PFOS dose-dependently induced a decrease in sperm count, low levels of testosterone, and damage in testicular interstitium morphology. In vitro models, PFOS significantly increased miR-9-3p levels in Sertoli cells and SC-Exo, accompanied by a decrease in testosterone secretion and StAR expression in Leydig cells when Leydig cells were exposed to SC-Exo. Meanwhile, inhibition of SC-Exo or miR-9-3p by their inhibitors significantly rescued PFOS-induced decreases in testosterone secretion and the mRNA and protein expression of the StAR gene in Leydig cells. In summary, the present study highlights the role of the SC-Exo/miR-9-3p/StAR signaling pathway in PFOS-induced suppression of testosterone biosynthesis, advancing our understanding of molecular mechanisms for PFOS-induced male reproductive disorders.

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.