The increasing use of rare earth elements (REEs) in various industries has led to a rise in discharge points, thus increasing discharge rates, circulation, and human exposure. Therefore, REEs have received widespread attention as important emerging pollutants. This article thus summarizes and discusses the distribution and occurrence of REEs in the world's soil and water, and briefly introduces current REEs content analysis technology for the examination of different types of samples. Specifically, this review focuses on the impact of REEs on plants, including the distribution and fractionation of REEs in plants and their bioavailability, the effect of REEs on seed germination and growth, the role of REEs in plant resistance, the physiological and biochemical responses of plants in the presence of REEs, including mineral absorption and photosynthesis, as well as a description of the substitution mechanism of REEs competing for Ca in plant cells. Additionally, this article summarizes the potential mechanisms of REEs to activate endocytosis in plants and provides some insights into the mechanisms by which REEs affect endocytosis from a cell and molecular biology perspective. Finally, this article discusses future research prospects and summarizes current scientific findings that could serve as a basis for the development of more sustainable rare earth resource utilization strategies and the assessment of REEs in the environment.

Facing the challenge of global microplastics (MPs) pollution, full characterization of MPs biohazards is urgent. Recent intensive studies revealed that the toxicity depends on the material, size, and exposure concentration of MP. To better elucidate MPs biohazards, we investigated the impact of polystyrene-MPs of size 0.1 μm at a low dose of 50 μg/L on the neuromuscular, retinal, and reproductive phenotypes of fruit fly model, by voltage-clamped electrophysiology, electroretinogram, and reproductive assay, respectively. We found that MPs decreased the frequency of spontaneous junction currents of synapse and altered the receptor potential amplitude of the retina. Furthermore, MPs lowered the rate of embryo-laying of fruit flies. The differential gene expression of ligand-receptor interaction, endocytosis, phototransduction, and Toll/Imd signaling pathways might underlie these MPs-induced phenotypes. These findings call for further investigation on the potential biohazards of low-dose MPs.

Inhalation represents the most prevalent route of exposure with Thorium-232 compounds (Th-nitrate/Th-dioxide)/Th-containing dust in real occupational scenario. The present study investigated the mechanism of Th response in normal human alveolar epithelial cells (WI26), exposed to Th-nitrate or colloidal Th-dioxide (1–100 μg/ml, 24–72 h). Assessment in terms of changes in cell morphology, cell proliferation (cell count), plasma membrane integrity (lactate dehydrogenase leakage) and mitochondrial metabolic activity (MTT reduction) showed that Th-dioxide was quantitatively more deleterious than Th-nitrate to WI26 cells. TEM and immunofluorescence analysis suggested that Th-dioxide followed a clathrin/caveolin-mediated endocytosis, however, membrane perforation/non-endocytosis seemed to be the mode of Th internalization in cells exposed to Th-nitrate. Th-estimation by ICP-MS showed significantly higher uptake of Th in cells treated with Th-dioxide than with Th-nitrate at a given concentration. Both Th-dioxide and nitrate were found to increase the level of reactive oxygen species, which seemed to be responsible for lipid peroxidation, alteration in mitochondrial membrane potential and DNA-damage. Amongst HSPs, the protein levels of HSP70 and HSP90 were affected differentially by Th-nitrate/dioxide. Specific inhibitors of ATM (KU55933) or HSP90 (17AAG) were found to increase the Th- cytotoxicity suggesting prosurvival role of these signaling molecules in rescuing the cells from Th-toxicity.

Attention has been paid to the environmental distribution and fate of nanomedicines. However, their effects on the toxicity of environmental pollutants are lack of knowledge. In this study, the negatively charged poly (ethylene glycol)-b-poly (L-lactide-co-glycolide) (mPEG-PLA) and positively charged polyethyleneimine-palmitate (PEI-PA) nanomicelles were synthesized and served as model drug carriers to study the interaction and combined toxicity with dichlorodiphenyltrichloroethane (DDT). DDT exerted limited effect on the biointerfacial behavior of mPEG-PLA nanomicelles, whereas it significantly mitigated the attachment of PEI-PA nanomicelles on the model cell membrane as monitored by quartz crystal microbalance with dissipation (QCM-D). The cytotoxicity of DDT towards NIH 3T3 cells was greatly decreased by either co-treatment or pre-treatment with the nanomicelles according to the results of real-time cell analysis (RTCA). The cell viability of NIH 3T3 exposed to DDT was increased up to 90% by the co-treatment with mPEG-PLA nanomicelles. Three possible reasons were proposed: (1) decreased amount of free DDT in the cell culture medium due to the partitioning of DDT into nanomicelles; (2) mitigated cellular uptake of nanomicelle-DDT complexes due to the complex agglomeration or electrostatic repulsion between complexes and cell membrane; (3) detoxification effect in the lysosome upon endocytosis of nanomicelle-DDT complexes.

Quantum dots (QDs) have attracted broad attention due to their special optical properties and promising prospect in medical and biological applications. However, the process of QDs on cell membrane is worth further investigations because such process may lead to harmful effects on organisms and also important for QD application. In this study, adhesion of amino- and carboxyl-coated CdTe QDs (A-QDs and C-QDs) on cell membrane and the subsequent internalization are studied using a series of endocytosis-free model membranes, including giant and small unilamellar vesicles, supported lipid bilayers and giant plasma membrane vesicles (GPMVs). The adhered QD amounts on model membranes are quantified by a quartz crystal microbalance. The CdTe QD adhesion on model membranes is governed by electrostatic forces. Positively charged A-QDs adhere on GPMV surface and passively penetrate the plasma membrane via endocytosis-free mechanism, but negatively charged C-QDs cannot. Rat basophilic leukemia (RBL-2H3) cells are exposed to CdTe QDs to monitor the QD internalization process. Both A- and C-QDs are internalized by RBL-2H3 cells mainly via endocytosis. CdTe QDs do not accumulate on the plasma membrane of living cells due to the fast endocytosis and the weakened electrostatic attraction in biological medium, resulting in low chance of passive penetration. The suspended cells after trypsin digestion take more QDs than the adherent cells. A-QDs cause lower cell viability than C-QDs, probably because the approach of positively charged QDs to cells is favored and the smaller aggregates of A-QDs.

Aggravating the pollution of microcystins (MCs) in freshwater environments is detrimental to aquatic living organisms and humans, and thus threatens the stability of ecosystems. Some environmental factors have been verified to promote the production of MCs in Microcystis aeruginosa, thereby aggravating the pollution of MCs. However, the effects of cerium (Ce), the most abundant rare earth element in global water environments, on the production of MCs in M. aeruginosa are unknown. Here, Lake Taihu water was selected as a representative of freshwater environments. By using interdisciplinary methods, it was found that: (1) the exposure level of Ce [Ce(III) and Ce(IV)] in Lake Taihu water is in the range of 0.271–0.282 μg/L; (2) Ce exposure in Lake Taihu water promoted the contents of three main MCs (MC-LR, MC-LW and MC-YR) in M. aeruginosa and water; (3) a cellular mechanism of Ce promoting the production of MCs in M. aeruginosa in Lake Taihu water was suggested: Ce enhanced endocytosis in cells of M. aeruginosa to promote the essential element uptake by M. aeruginosa for MC synthesis. Thus, Ce exposure in Lake Taihu water aggravates the pollution of MCs via enhancing endocytosis in cells of M. aeruginosa. The results provide reference for assessing the environmental risk of Ce in water environments, investigating the mechanism of the pollution of MCs induced by environmental factors, and developing strategies aimed at preventing and controlling the pollution of MCs.

Fipronil, a broad-spectrum chiral insecticide, has been documented to induce significant neurotoxicity to nontarget aquatic species; however, whether its neurotoxicity behaves enantioselectively and what molecular mechanisms correspond to the neurotoxicity remain unanswered. To date, few investigations have focused on the genomic mechanisms responsible for the enantioselective toxicity of chiral pesticides. The epigenetic modifications, especially DNA methylation, caused by the pesticides are also blind spot of the research works. Video tracking showed that R-fipronil exhibited more intense neurotoxicity, as well as the induction of more severe anxiety-like behavior, such as boosted swimming speed and dysregulated photoperiodic locomotion, to embryonic and larval zebrafish compared with S-fipronil. The MeDIP-Seq analysis, combined with Gene Ontology and KEGG, revealed that R-fipronil disrupted five signaling pathways (MAPK, Calcium signaling, Neuroactive ligand-receptor interaction, Purine metabolism, and Endocytosis) to a greater extent than S-fipronil through the hypermethylation of several important neuro-related genes, whereas no significant alterations of global DNA methylation were observed on the two enantiomers. To summarize, our data indicated that the fipronil-conducted enantioselective neurotoxicity likely applied its enantioselectivity by the dysregulation of DNA methylation. Our study also provided novel epigenetic insights into the study of enantioselective biological effects and the relevant underlying mechanisms of chiral insecticide.

Use of nanotechnology products is increasing; with silver (Ag) nanoparticles particularly widely used. A key uncertainty surrounding the risk assessment of AgNPs is whether their effects are driven through the same mechanism of action that underlies the toxic effects of Ag ions. We present the first full transcriptome study of the effects of Ag ions and NPs in an ecotoxicological model soil invertebrate, the earthworm Eisenia fetida. Gene expression analyses indicated similar mechanisms for both silver forms with toxicity being exerted through pathways related to ribosome function, sugar and protein metabolism, molecular stress, disruption of energy production and histones. The main difference seen between Ag ions and NPs was associated with potential toxicokinetic effects related to cellular internalisation and communication, with pathways related to endocytosis and cilia being significantly enriched. These results point to a common final toxicodynamic response, but initial internalisation driven by different exposure routes and toxicokinetic mechanisms.

Trace metals and broad-spectrum antibiotic drugs are common environmental contaminants, the importance of which is increasing due to global climate change-related effects.In the present study, the biological model organism E. crassus was first acclimated to five temperatures, from 25 °C to 33 °C, followed by exposure to nominal concentrations of copper, the antibiotic model compound oxytetracycline and mixtures of both, at increasing thermal conditions. Variations of temperature-related toxicity were assessed by two high-level endpoint tests, survival and replication rates, and two sublethal parameters: endocytosis rate and lysosomal membrane stability. The selected toxicants presented opposite behaviours as the protozoa's survival rates increased following an increasing thermal gradient in the oxytetracycline-related treatments, and a decline of tolerance in metal-related treatments was observed. Results of tests combining binary mixtures of tested toxicants showed a complex pattern of responses.

With the widespread use of plastics and nanotechnology products, nanoplastics (NPs) have become a potential threat to human health. It is of great practical significance to study and evaluate the distribution of NPs in mice as mammal models and their entry, transport, and cytotoxicity in human cell lines. In this study, we detected the tissue distribution of fluorescent polystyrene nanoplastics (PS-NPs) in mice and assessed their endocytosis, transport pathways, and cytotoxic effects in GES-1 cells. We found that PS-NPs were clearly visible in gastric, intestine, and liver tissues of mice and in GES-1 cells treated with PS-NPs. Entry of PS-NPs into GES-1 cells decreased with the inhibition of caveolae-mediated endocytosis (nystatin), clathrin-mediated endocytosis (chlorpromazine HCl), micropinocytosis (ethyl-isopropyl amiloride), RhoA (CCG-1423), and F-actin polymerization (lantrunculin A). Rac1 inhibitors (NSC 23766) had no significant effect on PS-NPs entering GES-1 cells. F-actin levels significantly decreased in CCG-1423-pretreated GES-1 cells exposed to PS-NPs. GES-1 cell ultrastructural features indicated that internalized PS-NPs can be encapsulated in vesicles, autophagosomes, lysosomes, and lysosomal residues. RhoA, F-actin, RAB7, and LAMP1 levels in PS-NPs-treated GES-1 cells were remarkably up-regulated and the Rab5 level was significantly down-regulated compared to levels in untreated cells. PS-NPs treatment decreased cell proliferation rates and increased cell apoptosis. The formation of autophagosomes and autolysosomes and levels of LC3II increased with the length of PS-NPs treatment. The results indicated that cells regulated endocytosis in response to PS-NPs through the RhoA/F-actin signaling pathway and internalized PS-NPs in the cytoplasm, autophagosomes, or lysosomes produced cytotoxicity. These results illustrate the potential threat of NPs pollution to human health.