Silver nanoparticles (AgNPs) of both biologically and chemically origins trigger various physiological and metabolic processes through interaction with plant cells, exerting positive, negative and inconsequential effects. However, their impacts on plant systems must be critically investigated to guarantee their safe application in food chain. In this study, the effects of chemically synthesized (synthetic) AgNPs (sAgNPs) and biologically synthesized (biogenic) AgNPs (bAgNPs) on physiological and biochemical features of Eschscholzia californica Cham were evaluated at different concentrations (0, 10, 25, 50 and 100 mg L⁻¹). Plants exposed to bAgNPs (at 10 and 25 mg L⁻¹) and sAgNPs (at 10 mg L⁻¹) displayed relatively uniform deposition of AgNPs on leaf surface, however, the higher concentration (100 mg L⁻¹) was accompanied by aggregation of AgNPs, resulting in anatomical and physiological disorders. Foliar application of both AgNPs at lower concentrations resulted in significant (P < 0.01) improve in the content of photosynthetic pigments (chlorophylls a, b, a+b, and carotenoids) and total phenolics over the control in a dose-related manner. Leaf relative water content decreased steadily with increasing both sAgNPs and bAgNPs concentrations-with sAgNPs being more inhibitive. Both types of AgNPs at 100 mg L⁻¹ significantly (P < 0.05) increased electrolyte leakage index, level of lipid peroxidation product (malondialdehyde), and leaf soluble sugar content when compared to controls. No significant difference was found on cell membrane stability index among the plants exposed to bAgNPs and sAgNPs at the lowest concentration over the control. Californidine content was significantly (P < 0.01, by 45.1%) increased upon all the bAgNPs treatments (with a peak at 25 mg L⁻¹) relative to control. The obtained extracts from plants treated with bAgNPs at lower concentrations revealed a significant induction of antioxidant capacity (based on DPPH˙ free radical scavenging and ferrous ions-chelating activities) with lower IC₅₀ values compared to the other treatments. Conclusively, bAgNPs at lower concentrations are potent elicitors of pharmaceutically active compounds biosynthesis, which enhance physiological efficiency of E. californica, but at higher concentrations bAgNPs are equally toxic as sAgNPs.

Application of nanopesticides may substantially increase surface attachment and internalization of engineered nanoparticles (ENPs) in food crops. This study investigated the role of stomata in the internalization of silver nanoparticles (Ag NPs) using abscisic acid (ABA)-responsive ecotypes (Ler and Col-7) and ABA-insensitive mutants (ost1-2 and scord7) of Arabidopsis thaliana in batch sorption experiments, in combination with microscopic visualization. Compared with those of the ABA-free control, stomatal apertures were significantly smaller for the Ler and Col-7 ecotypes (p ˂ 0.05) but remained unchanged for the ost1-2 and scord7 mutants, after exposure to 10 μM ABA for 1 h. Generally Ag NP sorption to the leaves of the Ler and Col-7 ecotypes treated with 10 μM ABA was lower than that in the ABA-free control, mainly due to ABA-induced stomatal closure. The difference in Ag NP sorption with and without ABA was less pronounced for Col-7 than for Ler, suggesting different sorption behaviors between these two ecotypes. In contrast, there was no significant difference in foliar sorption of Ag NPs by the ost1-2 and scord7 mutants with and without ABA treatment. Ag NPs were widely attached to the Arabidopsis leaf surface, and found at cell membrane, cytoplasm, and plasmodesmata, as revealed by scanning electron microscopy and transmission electron microscopy, respectively. These results highlight the important role of stomata in the internationalization of ENPs in plants and may have broad implications in foliar application of nanopesticides and minimizing contamination of food crops by ENPs.

The present study aims to explore the bioaccumulation and biotic transformations of inorganic (iHg) and monomethyl mercury (MMHg) by natural pico-nanoplankton community from eutrophic lake Soppen, Switzerland. Pico-nanoplankton encompass mainly bacterioplankton, mycoplankton and phytoplankton groups with size between 0.2 and 20 μm. Species-specific enriched isotope mixture of ¹⁹⁹iHg and ²⁰¹MMHg was used to explore the accumulation, the subcellular distribution and transformations occurring in natural pico-nanoplankton sampled at 2 different depths (6.6 m and 8.3 m). Cyanobacteria, diatoms, cryptophyta, green algae and heterotrophic microorganisms were identified as the major groups of pico-nanoplankton with diatoms prevailing at deeper samples. Results showed that pico-nanoplankton accumulated both iHg and MMHg preferentially in the cell membrane/organelles, despite observed losses. The ratios between the iHg and MMHg concentrations measured in the membrane/organelles and cytosol were comparable for iHg and MMHg. Pico-nanoplankton demethylate added ²⁰¹MMHg (~4 and 12% per day depending on cellular compartment), although the involved pathways are to further explore. Comparison of the concentrations of ²⁰¹iHg formed from ²⁰¹MMHg demethylation in whole system, medium and whole cells showed that 82% of the demethylation was biologically mediated by pico-nanoplankton. No significant methylation of iHg by pico-nanoplankton was observed. The accumulation of iHg and MMHg and the percentage of demethylated MMHg correlated positively with the relative abundance of diatoms and heterotrophic microorganisms in the pico-nanoplankton, the concentrations of TN, Mg²⁺, NO₃⁻, NO₂⁻, NH₄⁺ and negatively with the concentrations of DOC, K⁺, Na⁺, Ca²⁺, SO₄²⁻. Taken together the results of the present field study confirm the role of pico-nanoplankton in Hg bioaccumulation and demethylation, however further research is needed to better understand the underlying mechanisms and interconnection between heterotrophic and autotrophic microorganisms.

The B-type cyclin gene, CycB2, serves as a negative regulator of glandular trichome initiation. Through targeted knockout of NtCycB2 in Nicotiana tabacum cv. K326 using the CRISPR/Cas9 system, we created a variety, HK326, which exhibits significantly increased density and larger glandular heads of long glandular trichomes. Under Cd-stress, HK326 exhibited enhanced Cd tolerance, as demonstrated by a robust root system, strengthened cell membrane stability, and higher photosynthetic parameters. HK326 exhibited enhanced Cd-stress tolerance due to a strong excretion capacity of long glandular trichomes by forming calcium oxalate crystals. Cd mainly accumulated in tobacco shoots rather than remained in roots. Specifically, Cd levels of the HK326 shoot surface were nearly two-fold of those of K326, resulting in less Cd internally in the roots and shoots. Gene expression patterns revealed 11 Cd transporter genes that were upregulated after Cd-stress in shoots, roots, and trichomes. Among them, the NtHMA2 gene encoding heavy metal ATPases and involved in the transport of divalent heavy metal cations was expressed consistently and significantly higher in HK326 than K326, both before and after Cd-stress. NtHMA2 expression was strong in trichomes, moderate in shoots, while weak in roots. The results indicate that NtHMA2 may be involved in Cd excretion from glandular trichomes. Our findings suggest HK326 may be an appropriate candidate plant for Cd-stress tolerance.

Antibiotic resistance in environmental matrices becomes urgently significant for public health and has been considered as an emerging environmental contaminant. In this work, the ampicillin-resistant Escherichia coli (AR E. coli) and corresponding resistance genes (blaTEM₋₁) were effectively eliminated by the electrocatalytic process, and the dissemination risk of antibiotic resistance was also investigated. All the AR E. coli (∼8 log) was inactivated and 8.17 log blaTEM₋₁ was degraded by the carbon nanotubes/agarose/titanium (CNTs/AG/Ti) electrode within 30 min. AR E. coli was inactivated mainly attributing to the damage of cell membrane, which was attacked by reactive oxygen species and subsequent leakage of intracellular cytoplasm. The blaTEM₋₁ was degraded owing to the strand breaking in the process of electrocatalytic degradation. Furthermore, the dissemination risk of antibiotic resistance was effectively controlled after being electrocatalytic treatment. This study provided an effective electrocatalytic technology for the inactivation of antibiotic resistant bacteria and control of antibiotic resistance dissemination risk in the aqueous environment.

Discharged carbon nanotubes (CNTs) likely interact with co-existing organic contaminants (OCs) and pose joint toxicity to environmental microbes. Herein, hydrophobic pentachlorophenol (PCP) and hydrophilic ciprofloxacin (CIP) were used as representative OCs and their joint toxicities with CNTs to Bacillus subtilis were systematically investigated at cellular, biochemical, and omics levels. The 3-h bacterial growth half inhibitory concentrations of CNTs, PCP, and CIP were 12.5 ± 2.6, 3.5 ± 0.5, and 0.46 ± 0.03 mg/L, respectively, and they all could damage cell membrane, increase intracellular oxidative stress, and alter bacterial metabolomics and transcriptomics; while CNTs-PCP and CNTs-CIP binary exposures exhibited distinct additive and synergistic toxicities, respectively. CNTs increased bacterial bioaccumulation of PCP and CIP via destabilizing and damaging cell membrane. PCP reduced the bioaccumulation of CNTs, while CIP had no significant effect; this difference could be owing to the different effects of the two OCs on cell-surface hydrophobicity and CNTs electronegativity. The additive toxicity outcome upon CNTs-PCP co-exposure could be a result of the balance between the increased toxicity from increased PCP bioaccumulation and the decreased toxicity from decreased CNTs bioaccumulation. The increased bioaccumulation of CIP contributed to the synergistic toxicity upon CNTs-CIP co-exposure, as confirmed by the increased inhibition of topoisomerase Ⅳ activity and interference in gene expressions regulating ABC transporters and lysine biosynthesis. The findings provide novel insights into environmental risks of CNTs.

Nicosulfuron is a sulfonylurea family herbicide which is commonly applied together with the triazine herbicide atrazine in agricultural practice. However, whether nicosulfuron can influence the biodegradation of atrazine is unclear. Therefore, the influence of nicosulfuron on atrazine removal as well as on cell viability and transcription of atrazine chlorohydrolase gene (trzN) in Arthrobacter sp. DNS10 was investigated in this study. Our results demonstrated that 76.0% of atrazine was degraded in the absence of nicosulfuron after 48h of culture, whereas 63.9, 49.1 and 42.6% was degraded in the presence of 1, 5, and 10 mg/L of nicosulfuron, respectively. Nicosulfuron also induced an increase in the level of intracellular reactive oxygen species (ROS), thereby damaging the cell membrane integrity and inhibiting the growth of the strain DNS10. Flow cytometry analysis revealed that the cell viability of strain DNS10 decreased with an increase in nicosulfuron concentration. The transcription of trzN in strain DNS10 exposed to the three described levels of nicosulfuron was 0.99, 0.72 and 0.52 times, respectively, that without nicosulfuron. In brief, nicosulfuron could inhibit atrazine removal efficiency by strain DNS10 by inducing the over-production of ROS which ultimately enhances the population of membrane-damaged cells, as well as reducing cell viability and trzN transcription. The outcomes of the present study provide new insights into the mechanism of nicosulfuron inhibition on atrazine biodegradation by strain DNS10.

PM₂.₅ has a major impact on the gastrointestinal system, but the specific mechanism behind this action is not fully understood. Current studies have focused on the relationship between PM₂.₅ and intestinal flora disorder, while ignoring the important influence of diet on gut microbes. In this study, SD rats were fed either a normal, high-fat, or high-carbohydrate diet for two months and exposed to PM₂.₅ (7 mg/kg b.w.) by intratracheal instillation. The results showed that the body and kidney weights of the rats in the high-fat diet group were significantly increased relative to those with a normal diet, and changes in the intestinal microbes and metabolites induced by PM₂.₅ were observed. Rats in the high-carbohydrate diet group had a significant response, and the diversity and richness indices of the flora were reduced (p < 0.05); additionally, intestinal Biffidobacterium and Lactobacillus were enriched, while many endogenous metabolites were found. Some amino acids derivatives and long-chain fatty acids were increased (p < 0.05). Both diet structure and PM₂.₅ exposure can affect the composition of gut microbiota, and intestinal metabolites may be associated with cell membrane damage when a high-carbohydrate diet interacts with PM₂.₅. This study considers multiple dietary factors to further supplement the evidence of intestinal damage via PM₂.₅.

Here we investigated the acute effects (12 h exposure) of three polystyrene nanoplastics (PS NPs, including PS, PS−COOH and PS−NH₂) on extracellular polymeric substance (EPS) composition of activated sludge. Three PS NPs exhibited the significant inhibition in total EPS and protein (PRO) production. The functional groups involved in the interactions between PS NPs and EPS were C-(C, H), and those between PS-NH₂ NPs and EPS were CO and O–C–O. In addition, the dewaterability of activated sludge were optimized by three PS NPs, especially PS-NH₂ NPs. Three PS NPs caused nonnegligible cellular oxidative stress and cell membrane damage in activated sludge (PS NPs exposure concentration: 100 mg/L). Among them, the cell membrane damage caused by PS-NH₂ was the most significant. Overall, the degree of influence on EPS and cytotoxicity of activated sludge varies with the surface functional groups of PS NPs.

The surface modifications of nanoparticles (NPs), are well-recognized parameters that affect the toxicity, while there has no study on toxicity of Al₂O₃ NPs with different surface modification. Therefore, for the first time, this study pays attention to evaluating the toxicity and potential mechanism of pristine Al₂O₃ NPs (p-Al₂O₃), hydrophilic (w-Al₂O₃) and lipophilic (o-Al₂O₃) modifications of Al₂O₃ NPs both in vitro and in vivo. Applied concentrations of 10, 20, 40, 80,100 and 200 μg/mL for 24 h exposure on Caenorhabditis elegans (C. elegans), while 100 μg/mL of Al₂O₃ NPs significantly decreased the survival rate. Using multiple toxicological endpoints, we found that o-Al₂O₃ NPs (100 μg/mL) could induce more severe toxicity than p-Al₂O₃ and w-Al₂O₃ NPs. After uptake by C. elegans, o-Al₂O₃ NPs increased the intestinal permeability, easily swallow and further destroy the intestinal membrane cells. Besides, cytotoxicity evaluation revealed that o-Al₂O₃ NPs (100 μg/mL) are more toxic than p-Al₂O₃ and w-Al₂O₃. Once inside the cell, o-Al₂O₃ NPs could attack mitochondria and induce the over-production of reactive oxygen species (ROS), which destroy the intracellular redox balance and lead to apoptosis. Furthermore, the transcriptome sequencing and RT-qPCR data also demonstrated that the toxicity of o-Al₂O₃ NPs is highly related to the damage of cell membrane and the imbalance of intracellular redox. Generally, our study has offered a comprehensive sight to the adverse effects of different surface modifications of Al₂O₃ NPs on environmental organisms and the possible underlying mechanisms.