Bacteria and their secreted extracellular polymeric substances (EPS) are widely distributed in ecosystems and have high capacity for heavy metal immobilization. The knowledge about the molecular-level interactions with heavy metal ions is essential for predicting the behavior of heavy metals in natural and engineering systems. This comprehensive study using potentiometric titration, Fourier-transform infrared (FTIR) spectroscopy, isothermal titration calorimetry (ITC) and X-ray absorption fine structure (XAFS) was able to reveal the functional diversity and adsorption mechanisms for Pb onto bacteira and the EPS in greater detail than ever before. We identified mono-carboxylic, multi-carboxylic, phosphodiester, phosphonic and sulfhydryl sites and found the partitioning of Pb to these functional groups varied between gram-negative and gram-positive bacterial strains, the soluble and cell-bound EPS and Pb concentrations. The sulfhydryl and phosphodiester groups preferentially complexed with Pb in P. putida cells, while multifunctional carboxylic groups promoted Pb adsorption in B. subtilis cells and the protein fractions in EPS. Though the functional site diversity, the adsorption of Pb to organic ligands occurred spontaneously through a universal entropy increase and inner-sphere complexation mechanism. The functional group scale knowledge have implications for the modeling of heavy metal behavior in the environment and application of these biological resources.

The recently recognized adverse environmental and toxic effects of neonicotinoid insecticides (NNIs) on non-target organisms are alarming. A comprehensive design, screening, and regulatory system was developed to generate NNI derivatives and mutant receptors with selective-ecotoxicological effects to overcome such adverse effects. For ligand design, taking ACE-09 derivative as an example, the toxicity on non-target animals (aboveground: bees; underground: earthworms), plant absorption, and soil absorption decreased by 4.80% and 13.7%, 10.0%, and 121%, while the toxicity on target animals (aboveground: aphids; underground: B. odoriphagas), plant metabolism, and soil degradation increased by 70.2% and 51.7%, 5.08%, and 8.28%. For receptor modification, the ability of mutants to absorb ACE-09 derivative decreased by 31.0%, while the ability of mutants to metabolize ACE-09 derivative increased by 28.0% in scenario 2 (mainly plant selectivity); the ability of mutants to degrade ACE-09 derivative increased by 11.6% in scenario 3 (mainly soil selectivity). The above results indicated that the selective-ecotoxicological effects of ligand design and receptor modification were both improved. Additionally, the combined effects of the ACE-09 derivative on plant absorption and metabolic mutants improved by 31.1% and 31.4% in scenario 2, respectively, while the effect on microbial degradation mutant improved by 14.9%, indicating that there was a synergistic effect between ligand design and receptor modification. Finally, based on the interaction between the ACE-09 derivative and mutants, the optimal environmental factors that improved the selectivity of their ecotoxicological effects were determined. For example, alternate application of nitrogen and phosphorus fertilizers effectively reduced the oxidative damage to plants caused by NNI residues. The novel ligand-receptor joint modification method, combined with the regulation of environmental factors under multiple scenarios, can biochemically address the ecotoxicological concern and highlight the harmful effects of pesticides on the environment and non-target organisms.

Dioxybenzone is widely used in cosmetics and personal care products and frequently detected in multiple environmental media and human samples. However, the current understanding of the metabolic susceptibility of dioxybenzone and the potential endocrine disruption through its metabolites in mimicking human estrogens remains largely unclear. Here we investigated the in vitro metabolism of dioxybenzone, detected the residue of metabolites in rats, and determined the estrogenic disrupting effects of these metabolites toward estrogen receptor α (ERα). In vitro metabolism revealed two major metabolites from dioxybenzone, i.e., M1 through the demethylation of methoxy moiety and M2 through hydroxylation of aromatic carbon. M1 and M2 were both rapidly detected in rat plasma upon exposure to dioxybenzone, which were then distributed into organs of rats in the order of livers > kidneys > uteri > ovaries. The 100 ns molecular dynamics simulation revealed that M1 and M2 formed hydrogen bond to residue Leu387 and Glu353, respectively, on ERα ligand binding domain, leading to a reduced binding free energy. M1 and M2 also significantly induced estrogenic effect in comparison to dioxybenzone as validated by the recombinant ERα yeast two-hybrid assay and uterotrophic assay. Overall, our study revealed the potential of metabolic activation of dioxybenzone to induce estrogenic disrupting effects, suggesting the need for incorporating metabolic evaluation into the health risk assessment of benzophenones and their structurally similar analogs.

It has not been well understood that the binding affinity and potential toxicity of different chemical forms of selenite (Se(IV)), which are predominant forms of selenium with plant availability. The influences of pH and major anions on Se(IV) toxicity to wheat root elongation were determined in solutions and modeled based on the biotic ligand model (BLM) and free ion activity model (FIAM) concepts. Results showed that EC50[Se(IV)]T values increased from 164 to 273 μM as the pH raised from 4.5 to 8.0, indicating the increase of pH induced weakened Se(IV) toxicity. The EC50{SeO₃²⁻} values increased from 0.019 to 71.3 μM while the EC50{H₂SeO₃} values sharply decreased from 2.08 μM to 0.760 nM with the pH increasing from 4.5 to 8.0. The effect of pH on Se(IV) toxicity could be explained by the changes of Se(IV) species in different pH solutions as H₂SeO₃, HSeO₃⁻ and SeO₃²⁻ were differently toxic to wheat root elongation. The toxicity of Se(IV) decreased with increasing H₂PO₄⁻ activity but not for SO₄²⁻, NO₃⁻ and Cl⁻ activities, indicating that only H₂PO₄⁻ had a competitive effect with Se(IV) on the binding sites. A site-specific BLM was developed to count in effects of pH and H₂PO₄⁻, and stability constants of H₂SeO₃, HSeO₃⁻, SeO₃²⁻ and H₂PO₄⁻ to the binding sites were obtained: logKH2SeO3BL = 4.96, logKHSeO3BL = 3.47, logKSeO3BL = 2.56 and logKH2PO4BL = 2.00. Results implied that BLM performed much better than FIAM in the wheat root elongation prediction when coupling toxic species H₂SeO₃, HSeO₃⁻, SeO₃²⁻, and the competitions of H₂PO₄⁻ for the binding sites while developing the Se(IV)-BLM.

Imidacloprid (IMI) is widely used in agriculture, and is toxic to non-target aquatic species. Quercetin (Que) is a flavonoid abundant in fruits and vegetables that exhibits anti-oxidant activity. In the present study, we treated grass carp hepatocytes (L8824) with 0.1 μM Que and/or 1 mM IMI for 24 h to explore the effect of Que on IMI-induced mitochondrial apoptosis. We found that IMI exposure enhanced reactive oxygen species (ROS) generation, inhibiting the activities of SOD, CAT and T-AOC, exacerbating the accumulation of MDA, aggravating the expression of mitochondrial apoptosis pathway (Cyt-C, BAX, Caspase9 and Caspase3) related genes and decreased the expression of anti-apoptosis gene B-cell lymphoma-2 (Bcl-2). In addition, Que and IMI co-treatment significantly restored the activity of anti-oxidant enzymes, downregulated ROS level and apoptosis rate, thereby alleviating the depletion of mitochondrial membrane potential (ΔΨm) and the expression of cytochrome c (Cyt-C), Bcl-2-associated X (BAX), and cysteinyl aspartate specific proteinases (Caspase9 and 3), increasing the Bcl-2 level. Furthermore, we elucidated that Que could inhibit the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), thus activating phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway to attenuate IMI-induced apoptosis. Molecular docking provides assertive evidence for the interaction between Que ligand and PTEN receptor. Consequently, these results indicate that Que effectively antagonizes IMI-induced mitochondrial apoptosis in grass carp hepatocytes via regulating the PTEN/PI3K/AKT pathway.

Exposure to environmental endocrine disrupting chemicals (EDCs) is highly suspected in prostate carcinogenesis. Though, estrogenicity is the most studied behavior of EDCs, the androgenic potential of most of the EDCs remains elusive. This study investigates the androgen mimicking potential of some common EDCs and their effect in androgen-dependent prostate cancer (LNCaP) cells. Based on the In silico interaction study, all the 8 EDCs tested were found to interact with androgen receptor with different binding energies. Further, the luciferase reporter activity confirmed the androgen mimicking potential of 4 EDCs namely benzo[a]pyrene, dichlorvos, genistein and β-endosulfan. Whereas, aldrin, malathion, tebuconazole and DDT were reported as antiandrogenic in luciferase reporter activity assay. Next, the nanomolar concentration of androgen mimicking EDCs (benzo[a]pyrene, dichlorvos, genistein and β-endosulfan) significantly enhanced the expression of AR protein and subsequent nuclear translocation in LNCaP cells. Our In silico studies further demonstrated that androgenic EDCs also bind with epigenetic regulatory enzymes namely DNMT1 and HDAC1. Moreover, exposure to these EDCs enhanced the protein expression of DNMT1 and HDAC1 in LNCaP cells. These observations suggest that EDCs may regulate proliferation in androgen sensitive LNCaP cells by acting as androgen mimicking ligands for AR signaling as well as by regulating epigenetic machinery. Both androgenic potential and epigenetic modulatory effects of EDCs may underlie the development and growth of prostate cancer.

Because the pollutants produced by human activities have destroyed the ecological balance of natural water environment, and caused severe impact on human life safety and environmental security. Hence the task of water environment restoration is imminent. Metal-organic frameworks (MOFs), structured from organic ligands and inorganic metal ions, are notable for their outstanding crystallinity, diverse structures, large surface areas, adsorption performance, and excellent component tunability. The water stability of MOFs is a key requisite for their possible actual applications in separation, catalysis, adsorption, and other water environment remediation areas because it is necessary to safeguard the integrity of the material structure during utilization. In this article, we comprehensively review state-of-the-art research progress on the promising potential of MOFs as excellent nanomaterials to remove contaminants from the water environment. Firstly, the fundamental characteristics and preparation methods of several typical water-stable MOFs include UiO, MIL, and ZIF are introduced. Then, the removal property and mechanism of heavy metal ions, radionuclide contaminants, drugs, and organic dyes by different MOFs were compared. Finally, the application prospect of MOFs in pollutant remediation prospected. In this review, the synthesis methods and application in water pollutant removal are explored, which provide ways toward the effective use of water-stable MOFs in materials design and environmental remediation.

The synergistic cooperation of microbial cells and their extracellular polymeric substances (EPS) in biofilms is critical for the biofilm’s resistance to heavy metals and the migration and transformation of heavy metals. However, the effects of different components of biofilms have not been fully understood. In this study, the spatial distribution and speciation of copper in the colloidal EPS, capsular EPS, cell walls and membranes, and intracellular fraction of unsaturated Pseudomonas putida (P. putida) CZ1 biofilms were fully determined at the subcellular level. It was found that 60–67% of copper was located in the extracellular fraction of biofilms, with 44.7–42.3% in the capsular EPS. In addition, there was 15.5–20.1% and 17.2–21.2% of copper found in the cell walls and membranes or the intracellular fraction, respectively. Moreover, an X-ray absorption fine structure spectra analysis revealed that copper was primarily bound by carboxyl-, phosphate-, and hydrosulfide-like ligands within the extracellular polymeric matrix, cell walls and membranes, and intracellular fraction, respectively. In addition, macromolecule quantification, fourier-transform infrared spectroscopy spectra and sulfur K-edge x-ray absorption near edge structure analysis further showed the carboxyl-rich acidic polysaccharides in EPS, phospholipids in cell walls and cell membranes, and thiol-rich intracellular proteins were involved in binding of copper in the different components of biofilm. The full understanding of the distribution and chemical species of heavy metals in biofilms not only promotes a deep understanding of the interaction mechanisms between biofilms and heavy metals, but also contributes to the development of effective biofilm-based heavy metal pollution remediation technologies.

Bisphenol A (BPA) and bisphenol F (BPF) are widely distributed in the environment and daily consumptions, leading to exposure toward human and environmental animals. The potential risk of bisphenol analogs on pigment and skin health is not well documented. In this study, we found that 0.05 mg/L BPF (tolerated daily intake (TDI) value of BPA) affected the particle size and color density of zebrafish melanin. While BPA caused less depigmentation effect toward zebrafish with effective concentration of 5.0 mg/L. The downregulation of melanin synthases induced by BPF is associated with the reduction in melanin. Molecular dynamics indicated that both BPF and BPA could act as ligands of zebrafish and human Tyr family proteins; however, these compounds have completely different energetics and spatial steric effects, potentially explaining their varying depigmentation effects. Additionally, an in vitro assay using A375 melanoma cells demonstrated that the inhibitory effect of BPF on human melanin production was primarily attributed to Tyr inhibition. These findings provide an important basis for understanding the molecular mechanisms of BPF and BPA in melanin inhibition, and the results reflect the skin pigmentation interference risk of these compounds, which are ubiquitous in everyday personal products.

The use of polymers such as plastic has become an important part of daily life, and in aqueous environments, these polymers are considered as pollutants. When macropolymers are reduced to the nanoscale, their small particle size and large specific surface area facilitate their uptake by plants, which has a significant impact on aquatic plants. Therefore, it is essential to study the pollution of nanoscale polymers in the aquatic environment. In this work, we prepared nanoscale polymer dots (Pdots) and explored their toxicity, uptake and transport mechanisms in penny grass. From toxicological studies, in the absence of other nutrients, the cell structure, physiological parameters (total soluble protein and chlorophyll) and biochemical parameters (malondialdehyde) do not show significant changes over at least five days. Through in vivo fluorescence and photoacoustic (PA) imaging, the transport location can be visually detected accurately, and the transport rate can be analyzed without destroying the plants. Moreover, through ex vivo fluorescence imaging, we found that different types of Pdots have various uptake and transport mechanisms in stems and blades. It may be due to the differences in ligands, particle sizes, and oil-water partition coefficients of Pdots. By understanding how Pdots interact with plants, a corresponding method can be developed to prevent them from entering plants, thus avoiding the toxicity from accumulation. Therefore, the results of this study also provide the basis for subsequent prevention work.