The intestine is not only the main accumulation organ of microplastics (MPs), but also the intestinal environment is very conductive to the release of additives in MPs. However, the kinetics of release process, influence factors, and the related effects on gut microbiota remain largely unknown. In this study, a mucosal-simulator of the human intestinal microbial ecosystem (M-SHIME) was used to investigate the influence of gut microbiota on the release of phthalates (PAEs) from MPs and the effects of MPs on the intestinal luminal microbiota and mucosal microbiota. We found that di-(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and dimethyl phthalate (DMP) were the dominant PAEs released in the gut. Gut microbiota accelerated the release of PAEs, with the time to reach the maximum release was shortened from 7 days to 2 days. Moreover, MPs induced differential effects on luminal microbiota and mucosal microbiota. Compared with mucosal microbiota, the luminal microbiota was more susceptible to the leaching of PAEs from MPs, as evidenced by more microbiota alterations. MPs also inhibited the metabolic activity of intestinal flora based on the reduced production of short chain fatty acids (SCFA). These effects were mainly contributed by the release of PAEs. Acidaminococcus and Morganella were simultaneously correlated to the release of PAEs and the inhibition of metabolic activity of intestinal microbiota and can be used as indicators for the intestinal exposure of MPs and additives.

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.

The overnight stagnation of tap water in plumbing systems can lead to water quality deterioration. Meanwhile, the indoor heating can improve the indoor temperature in cold areas during winter, which may affect the quality of tap water during stagnation. However, indoor heating drives bacterial ecological links with tap water stagnation during winter are not well understood. The results indicated that the water temperature increased significantly after stagnation during indoor heating periods. Moreover, the average intact cell number and total adenosine triphosphate (ATP) concentration increased 1.53-fold and 1.35-fold after stagnation, respectively (P < 0.01). In addition, the increase in the ATP per cell number indicated that the combined effects of stagnation and indoor heating could enhance the bacterial activity. Biolog data showed that the bacterial community metabolic capacity was significantly higher in stagnant water than that of fresh water. Co-occurrence networks suggested that the bacterial metabolic profile changed after stagnation during the heating periods. DNA analysis indicated that the composition of the bacterial community changed dramatically after stagnation. The abundances of potential pathogens such as Mycobacterium sp. and Pseudomonas sp. also increased after stagnation. These results will give novel insights on comprehensive understanding the combined effects of indoor heating and overnight stagnation on the water bacterial community ecology of plumbing systems, and provide a scientific basis for tap water quality management after overnight stagnation during the indoor heating periods.

The typical alkyl organophosphorus flame retardant tributyl phosphate (TnBP) can leak from common products into the marine environment, with potential negative effects on marine organisms. However, risk assessments for TnBP regarding zooplankton are lacking. In this study, a marine rotifer, Brachionus plicatilis, was used to analyze the effect of TnBP (0.1 μg/L, environmental concentration; 1 and 6 mg/L) on reproduction, population growth, oxidative stress, mitochondrial function and metabolomics. Mortality increased as the TnBP concentration rose; the 24-h LC₅₀ value was 12.45 mg/L. All tested TnBP concentrations inhibited B. plicatilis population growth, with reproductive toxicity at the higher levels. Microstructural imaging showed ovary injury, the direct cause of reproductive toxicity. Despite elevated glutathione reductase activities, levels of reactive oxygen species and malonyldialdehyde increased under TnBP stress, indicating oxidative imbalance. TnBP induced mitochondrial malformation and activity suppression; the ROS scavenger N-acetylcysteine alleviated this inhibition, suggesting an internal connection. Nontargeted metabolomics revealed 398 and 583 differentially expressed metabolites in the 0.1 μg/L and 6 mg/L treatments relative to control, respectively, which were enriched in the pathways such as biosynthesis of amino acids, purine metabolism, aminoacyl-tRNA biosynthesis. According to metabolic pathway analysis, oxidative stress from purine degradation, mitochondrial dysfunction, disturbed lipid metabolism and elevated protein synthesis were jointly responsible for reproduction and population growth changes. This study echoes the results previously found in rotifer on trade-off among different life processes in response to environmental stress. Our systematic study uncovers the TnBP toxic mode of action.

Cyclophosphamide (CP) is an antineoplastic drug widely used in chemotherapy treatments with high consumption rates and that has been detected in the aquatic environment. After being released into the aquatic environment, CP may cause adverse effects on aquatic organisms since antineoplastics are well-known cytotoxic, genotoxic, mutagenic and teratogenic drugs. Moreover, predicted environmental changes, such as the temperature rising, may alter the impacts caused by CP on organisms. Thus, the present study aimed to assess the effects caused by CP chronic exposure in the mussel Mytilus galloprovincialis, under actual and predicted warming scenarios. Organisms were exposed for 28 days to different concentrations of CP (10, 100, 500 and 1000 ng/L) at control (17 ± 1.0 °C) and increased (21 ± 1.0 °C) temperatures. Biochemical responses related to metabolic capacity, energy reserves, oxidative stress and neurotoxicity were assessed. The results showed that the organisms were able to maintain their metabolic capacity under all exposure conditions. However, their antioxidant defense mechanisms were activated mostly at higher CP concentrations being able to prevent cellular damage, even under the warming scenario. Overall, the present findings suggest that temperature rise may not alter the impacts of CP towards M. galloprovincialis.

In this study, functional microbial sequencing, quantitative PCR, and phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) were employed to understand the microbial mechanisms related to the effects of bamboo charcoal (BC) and bamboo vinegar (BV) on the degradation of organic matter (OM) and methane (CH₄) emissions during composting. BC + BV resulted in the highest degradation of OM. BV was most effective treatment in controlling CH₄ emissions and it significantly reduced the abundance of the mcrA gene. Methanobrevibacter, Methanosarcina, and Methanocorpusculum were closely related to CH₄ emissions during the thermophilic composting period. PICRUSt analysis showed that BC and/or BV enhanced the metabolism associated with OM degradation and reduced CH₄ metabolism. Structural equation modeling indicated that BC + BV strongly promoted the metabolic activity of microorganisms, which had a positive effect on CH₄ emissions. Together these results suggest that BC + BV may be a suitable composting strategy if the aerobic conditions can be effectively improved during the thermophilic composting period.

Wild fish living downstream of wastewater treatment plants (WWTPs) often have increased body condition factors or body mass indices compared to upstream fish. This observation has been largely attributed to increased nutrient loading and food availability around wastewater effluent outflows. While a higher condition factor in fish is generally considered a predictor of healthy ecosystems, the metabolic status and capacity of the animals downstream of WWTPs may be a better predictor of fitness and potential population level effects. To address this, we sampled wild longnose dace (Rhinichthys cataractae), a native species in North American waterways, from sites upstream and downstream of WWTPs. Downstream fish had higher body mass indices, which corresponded with higher nutrient (lipid, protein, and glycogen) storage in somatic tissues compared to upstream fish. Liver transcriptome analysis revealed metabolic reprogramming favoring lipid synthesis, including higher hepatic triglyceride levels and transcript abundance of targeted lipogenic genes. This suggests that effluent exposure-mediated obesity in dace is a result of changes at the transcriptional level. To determine potential ecological consequences, we subjected these fish to an acute stressor in situ to determine their stress performance. Downstream fish failed to mobilize metabolites post-stress, and showed a reduction in liver aerobic and anaerobic metabolic capacity. Taken together, fish living downstream of WWTPs exhibit a greater lipid accumulation that results in metabolic disruption and may compromise the ability of these fish to cope with subsequent environmental and/or anthropogenic stressors.

Potassium (K⁺) is the most abundant cation in phytoplankton cells, but its impact on Microcystis aeruginosa (M. aeruginosa) has not been fully documented. This study presents evidence of how K⁺ availability affects the growth, oxidative stress and microcystin (MC) production of M. aeruginosa. The iTRAQ-based proteomic analysis revealed that during K⁺ deficiency, serious oxidative damage occurred and the photosynthesis-associated and ABC transporter-related proteins in M. aeruginosa were substantially downregulated. In the absence of K⁺, a 69.26% reduction in cell density was shown, and both the photosynthesis and iron uptake were depressed, which triggered a declined production of ATP and expression of MC synthetases genes (mcyA, B and D), and MC exporters (mcyH). Through the impairment of both the MC biosynthesis and MC transportation out of cells, K⁺ depletion caused an 85.89% reduction of extracellular MC content at the end of the study. However, with increasing in the available K⁺ concentrations, photosynthesis efficiency, the expression of ABC-transporter proteins, and the transcription of mcy genes displayed slight differences compared with those in the control group. This work represents evidence that K⁺ availability can regulate the physiological metabolic activity of M. aeruginosa and K⁺ deficiency leads to depressed growth and MC production in M. aeruginosa.

Wastewater containing high concentrations of nitriles, if discharged without an appropriate nonhazardous disposal strategy, will cause serious environmental pollution. During secondary sewage biological treatment, most existing bacteria cannot endure high-concentration nitriles due to poor tolerance and low degradation ability. The Rhodococcus rhodochrous strain BX2 screened by our laboratory shows high resistance to nitriles and can efficiently degrade these compounds. Compared with sole high-concentration nitriles present in the biodegradation process, the addition of glucose at a suitable concentration can effectively increase the biomass of BX2, promote the expression of nitrile-degrading enzyme genes, improve the activities of these enzymes and enhance the pollutant removal efficiency via carbon catabolite repression (CCR) mechanisms. Whole-genome sequencing revealed that the four key regulators of CCR identified in gram-negative and gram-positive bacteria are concomitant in BX2. This study provides an economically feasible strategy for the microbial remediation of high-concentration nitriles and other organic pollutants.

To compare aquatic organisms’ responses to the toxicity of copper oxide (CuO) nanoparticles (NPs) with those of CuO microparticles (MPs) and copper (Cu) ions, a global metabolomics approach was employed to investigate the changes of both polar and nonpolar metabolites in microalga Chlorella vulgaris after 5-day exposure to CuO NPs and MPs (1 and 10 mg/L), as well as the corresponding dissolved Cu ions (0.08 and 0.8 mg/L). Unchanged growth, slight reactive oxygen species production, and significant membrane damage (at 10 mg/L CuO particles) in C. vulgaris were demonstrated. A total of 75 differentiated metabolites were identified. Most metabolic pathways perturbed after CuO NPs exposure were shared by those after CuO MPs and Cu ions exposure, including accumulation of chlorophyll intermediates (max. 2.4–5.2 fold), membrane lipids remodeling for membrane protection (decrease of phosphatidylethanolamines (min. 0.6 fold) and phosphatidylcholines (min. 0.2–0.7 fold), as well as increase of phosphatidic acids (max. 1.5–2.9 fold), phosphatidylglycerols (max. 2.2–2.3 fold), monogalactosyldiacylglycerols (max. 1.2–1.4 fold), digalactosylmonoacylglycerols (max. 1.9–3.8 fold), diacylglycerols (max. 1.4 fold), lysophospholipids (max. 1.8–3.0 fold), and fatty acids (max. 3.0–6.2 fold)), perturbation of glutathione metabolism induced by oxidative stress, and accumulation of osmoregulants (max. 1.3–2.6 fold) to counteract osmotic stress. The only difference between metabolic responses to particles and those to ions was the accumulation of fatty acids oxidation products: particles caused higher fold changes (particles/ions ratio 1.9–3.0) at 1 mg/L and lower fold changes (particles/ions ratio 0.4–0.7) at 10 mg/L compared with ions. Compared with microparticles, there was no nanoparticle-specific pathway perturbed. These results confirm the predominant role of dissolved Cu ions on the toxicity of CuO NPs and MPs, and also reveal particle-specific toxicity from a metabolomics perspective.