Various microplastics (MPs) are found in the environment and organisms. MP residues in organisms can affect health; however, their impacts on metabolism in aquatic organisms remain unclear. In this study, zebrafish embryos were exposed to polyethylene MPs with sizes ranging from 1 to 4 μm at concentrations of 0, 10, 100, and 1000 μg/L for 7 days. Through qPCR technology, the results indicated that zebrafish exposed to polyethylene MPs exhibited significant change in microbes of the phyla Firmicutes, Bacteroidetes, Proteobacteria, and Verrucomicrobia, etc. Moreover, 16S RNA gene sequencing revealed that there was a significant difference in alpha diversity between the control and 1000 μg/L MP-treated groups. At the genus level, the abundance of Aeromonas, Shewanella, Microbacterium, Nevskia and Methyloversatilis have increased remarkably. Conversely, the abundance of Pseudomonas, Ralstonia and Stenotrophomonas were significant reduction after MPs exposure. In addition, the levels of TG (triglyceride), TCHO (total cholesterol), NEFA (nonesterified fatty acid), TBA (total bile acid), GLU (glucose) and pyruvic acid significantly changed in MP-treated larval zebrafish, indicating that their metabolism was disturbed by MPs. Transcriptional levels of glucose and lipid metabolism-related genes showed a decreasing trend. Furthermore, LC/MS-based nontargeted metabolomics analysis demonstrated that a total of 59 phospholipid-related substances exhibited significant changes in larval fish treated with 1000 μg/L MPs. The mRNA levels of phospholipid metabolism-related genes were also obviously changed. Pearson correlation analysis indicated that the abundance of Aeromonas, Shewanella and Chitinibacter bacteria showed a negative correlation with most phospholipids, while Nevskia, Parvibacter and Lysobacter showed a positive correlation with most phospholipids. Based on these results, it is suggested that 1–4 μm PE-MPs could impact the microbiome and metabolism of larval zebrafish. All of these results indicated that the health risk of MPs cannot be ignored.

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.

Silica nanoparticles (SiO2 NPs) can cause health hazard after their release into the environment. Adsorption of natural organic matter and biomolecules on SiO2 NPs alters their surface properties and cytotoxicity. In this study, SiO2 NPs were treated by bovine serum albumin (BSA) and humic acid (HA) to study their effects on the integrity and fluidity of model cell membranes. Giant and small unilamellar vesicles (GUVs and SUVs) were prepared as model cell membranes in order to avoid the interference of cellular activities. The microscopic observation revealed that the BSA/HA treated (BSA-/HA-) SiO2 NPs took more time to disrupt membrane than untreated-SiO2 NPs, because BSA/HA adsorption covered the surface SiOH/SiO- groups and weakened the interaction between NPs and phospholipids. The deposition of SiO2 NPs on membrane was monitored by a quartz crystal microbalance with dissipation (QCM-D). Untreated- and HA-SiO2 NPs quickly disrupted the SUV layer on QCM-D sensor; BSA-SiO2 NPs attached on the membranes but only caused slow vesicle disruption. Untreated-, BSA- and HA-SiO2 NPs all caused the gelation of the positively-charged membrane, which was evaluated by the generalized polarity values. HA-SiO2 NPs caused most serious gelation, and BSA-SiO2 NPs caused the least. Our results demonstrate that the protein adsorption on SiO2 NPs decreases the NP-induced membrane damage.

Environmental exposure to 2,3,7,8-tetrachlorodibenzofuran (TCDF), one of typical persistent organic pollutants (POPs) produced from municipal waste combustion, exerts toxic effects on human healthy. In the current study, we mainly used targeted metabolomics combined with untargeted ¹H NMR-based metabolomics to investigate the effects of TCDF exposure on lipid homeostasis in mice. We found that TCDF exposure induced hepatic lipogenesis, the early-stage of non-alcoholic fatty liver disease, manifested by excessive lipids including triglycerides, fatty acids and lipotoxic ceramides accumulated in the liver together with elevated serum very low-density lipoprotein by activating the aryl hydrocarbon receptor (AHR) and its target genes such as Cyp1a1 and Cd36. We also found that TCDF exposure induced alteration of phospholipids and choline metabolites and endoplasmic reticulum (ER) markers in the liver of mice, indicating that disruption of host cell membrane structural integrity and ER stress leading to hepatic steatosis. In addition, complementary information was also obtained from histopathologic assessments and biological assays, strongly supporting toxic effects of TCDF. These results provide new evidence of TCDF toxicity associated with fatty liver disease and further our understanding of health effects of environmental pollutants exposure.

Propamocarb (PM) is a widely used fungicide with property of affecting fatty acid and phospholipid biosynthesis in funguses. In this study, we explored its effects on mice gut microbiota and metabolism by exposing mice to 3, 30, and 300 mg/L PM through drinking water for a duration of 28 days. We observed that the transcription of hepatic genes related to regulate lipid metabolism were perturbed by PM exposure. The microbiota in the cecal contents and feces changed during or after PM exposure at phylum or genus levels. 16S rRNA gene sequencing for the cecal content revealed shifted in overall microbial structure after PM exposure, and operational taxonomic unit (OTU) analysis indicated that 32.2% of OTUs changed by 300 mg/mL PM exposure for 28 days. In addition, based on 1H NMR analysis,a total of 20 fecal metabolites mainly including succinate, short chain fatty acids, bile acids and trimethylamine were found to be significantly influenced by exposure to 300 mg/L PM.,. These metabolites were tightly correlated to host metabolism. Our findings indicated that high doses of PM exposure could disturb mice metabolism through, or partly through, altering the gut microbiota and microbial metabolites.

Nostoc sp. PCC 7120 (Nostoc), a typical filamentous cyanobacterium ubiquitous in aquatic system, is recognized as a model organism to study prokaryotic cell differentiation and nitrogen fixation. In this study, Nostoc cells incubated with arsenite (As(III)) for two weeks were extracted with dichloromethane/methanol (DCM/MeOH) and the extract was partitioned between water and DCM. Arsenic species in aqueous and DCM layers were determined using high performance liquid chromatography - inductively coupled plasma mass spectrometer/electrospray tandem mass spectrometry (HPLC-ICPMS/ESIMSMS). In addition to inorganic arsenic (iAs), the aqueous layer also contained monomethylarsonate (MAs(V)), dimethylarsinate (DMAs(V)), and the two arsenosugars, namely a glycerol arsenosugar (Oxo-Gly) and a phosphate arsenosugar (Oxo-PO4). Two major arsenosugar phospholipids (AsSugPL982 and AsSugPL984) were detected in DCM fraction. Arsenic in the growth medium was also investigated by HPLC/ICPMS and shown to be present mainly as the inorganic forms As(III) and As(V) accounting for 29%–38% and 29%–57% of the total arsenic respectively. The total arsenic of methylated arsenic, arsenosugars, and arsenosugar phospholipids in Nostoc cells with increasing As(III) exposure were not markedly different, indicating that the transformation to organoarsenic in Nostoc was not dependent on As(III) concentration in the medium. Our results provide new insights into the role of cyanobacteria in the biogeochemical cycling of arsenic.

Glyphosate-based herbicide (GBH) is the most widely used herbicide worldwide and has long been considered to have significantly low toxicity to non-target soil invertebrates based on short-term toxicity tests (<56 d). However, long-term GBH toxicity assessment is necessary as GBH is repeatedly applied in the same field annually because of the advent of glyphosate-resistant crops. In this study, a multigeneration test was conducted where Allonychiurus kimi (Collembola) was exposed to GBH for three generations (referred to as F₀, F₁, and F₂) to evaluate the long-term toxic effect. The endpoints used were adult survival and juvenile production for the individual level toxicity assessment. Phospholipid profile and population age structure were the endpoints used for sub-individual and population levels, respectively. GBH was observed to have no negative effects on adult survivals of all generations, but juvenile production was found to decrease in a concentration-dependent manner, with EC₅₀s being estimated as 572.5, 274.8, and 59.8 mg a.i. kg⁻¹ in the F₀, F₁, and F₂ generations, respectively. The age structure of A. kimi population produced in the test of all generations was altered by GBH exposure, mainly because of the decrease in the number of young juveniles. Further, differences between the phospholipid profiles of the control and GBH treatments became apparent over generations, with PA 16:0, PA 12:0, and PS 42:0 lipids not being detected at the highest concentration of 741 mg kg⁻¹ in F₂. Considering all our findings from sub-individual to population levels, repeated and long-term use of GBH could have significantly higher negative impacts on non-target soil organisms than expected.

High phosphorus (P) load and consequent algal bloom are critical issues because of their harmful effects to aquatic ecosystems. The organic phosphorus (Po) cycling and hydrolyzation pathway in the sediments of a hypereutrophic lake area with high algae biomass were investigated using stable isotopes (δ¹³C and δ¹⁵N) along with C/N ratios, a sequential extraction procedure, ³¹P NMR spectrum, and alkaline phosphatase activity (APA) was measured simultaneously. C/N ratios lower than 10 combined with lighter δ¹³C (−23.5 to −25.2‰) and δ¹⁵N values (3.7–9.5‰) indicated that endogenous algal debris contributed to the predominant proportions of P-containing organic matter in the sediments. Sequential extraction results showed that Po fractions decreased as nonlabile Po > moderately labile Po > biomass-Po. Decreasing humic-associated Po (HA-Po) in sediments downward suggested the degradation of high-molecular-weight Po compounds on the geological time scale to low-molecular-weight Po including fulvic-associated Po (FA-Po), which is an important source of labile Po in the sediment. An analysis of the solution ³¹P NMR spectrum analysis showed that important Po compound groups decreased in the order of orthophosphate monoesters > DNA-Po > phospholipids. The significant correlation indicated that orthophosphate monoesters were the predominant components of HA-Po. Rapid hydrolysis of labile orthophosphate diesters further facilitated the accumulation of orthophosphate monoesters in the sediments. Additionally, the simultaneously upward increasing trend demonstrated that APA accelerated the mineralization of Po into dissolved reactive phosphorus (DRP), which might feed back to eutrophication in algae-dominant lakes. The significantly low half-life time (T₁/₂) for important Po compound groups indicated faster metabolism processes, including hydrolysis and mineralization, in hypereutrophic lakes with high algae biomass. These findings provided improved insights for better understanding of the origin and cycling processes as well as management of Po in hypereutrophic lakes.

As an important part of extracellular secondary metabolites, extracellular polymeric substances (EPS) can play a significant role in protecting cells from the threat of exogenous substances, including nanoparticles (NPs). However, the regulation mechanisms of EPS secretion under NPs exposure remain largely unknown. This study investigated the signaling pathways and molecular responses related to EPS secretion of algae (Chlorella pyrenoidosa) upon the exposures to anatase and rutile TiO₂ NPs (nTiO₂-A and nTiO₂-R, respectively) at two similar toxic (20% and 50% of algal growth inhibition) concentrations. The results showed that EPS responded to nTiO₂ stress via excess secretion and compositional variation, and nTiO₂-A induced more EPS secretion than nTiO₂-R at similar toxicity concentrations. The up-regulation of the Ca²⁺ signaling pathway might play a greater role in promoting EPS secretion under nTiO₂-R exposure compared with nTiO₂-A exposure, while the significantly increased intracellular ROS could mainly account for the increased EPS secretion under nTiO₂-A exposure. The up-regulated genes related to biological synthesis and protein metabolism and the enhanced biosynthetic metabolism might be the direct causes of the increased EPS secretion. The increased ROS could have a greater effect on the amino acid metabolism and related genes upon the exposure to nTiO₂-A than nTiO₂-R to induce more EPS secretion. More serious membrane damage caused by nTiO₂-R than nTiO₂-A would affect the intracellular inositol phospholipid metabolism more severely, while the inositol phospholipid pathway and Ca²⁺ signaling pathway might agree and communicate with each other inherently to regulate EPS secretion upon nTiO₂-R exposure. The findings address the regulation mechanisms of algal EPS secretion under nTiO₂ exposure and provide new insights into algal bio-responses to nTiO₂ exposure.

The combined toxicity of mixed chemicals is usually evaluated according to several specific endpoints, and other potentially toxic effects are disregarded. In this study, we provided a metabolomics strategy to achieve a comprehensive understanding of toxicological interactions between mixed chemicals on metabolism. The metabolic changes were quantified by a pseudotargeted analysis, and the types of combined effects were quantitatively discriminated according to the calculation of metabolic effect level index (MELI). The metabolomics strategy was used to assess the combined effects of polycyclic aromatic hydrocarbons (PAHs) and short-chain chlorinated paraffins (SCCPs) on the metabolism of human hepatoma HepG2 cells. Our data suggested that exposure to a combination of PAHs and SCCPs at human internal exposure levels could result in an additive effect on the overall metabolism, whereas diverse joint effects were observed on various metabolic pathways. The combined exposure could induce a synergistic up-regulation of phospholipid metabolism, an additive up-regulation of fatty acid metabolism, an additive down-regulation of tricarboxylic acid cycle and glycolysis, and an antagonistic effect on purine metabolism. SCCPs in the mixture acted as the primary driver for the acceleration of phospholipid and fatty acid metabolism. Lipid metabolism disorder caused by exposure to a combination of PAHs and SCCPs should be an important concern for human health.