Numerous applications exist for graphene-based materials, such as graphene oxide (GO) nanosheets. Increased concentrations of GO nanosheets in the environment have the potential to have a large negative effect on the aquatic environment, with consequences for benthic organisms, such as polychaetes. The polychaete Hediste diversicolor mobilises the sediments, hence altering the availability of contaminants and the nutrients biogeochemical cycle. As such, this study proposes to assess the effects of different GO nanosheet concentrations on the behaviour, feeding activity, mucus production, regenerative capacity, antioxidant status, biochemical damage and metabolism of H. diversicolor. This study evidenced that H. diversicolor exposed to GO nanosheets had a significantly lower ability to regenerate their bodies, took longer to feed and burrow into the sediment and produced more mucus. Membrane oxidative damage (lipid peroxidation) increased in exposed specimens. The increased metabolic rate (ETS) evidenced a higher energy expenditure in exposed organisms (high use of ready energy sources – soluble sugars) to fight the toxicity induced by GO nanosheets, such as SOD activity. The increase in SOD activity was enough to reduce reactive oxygen species (ROS) induced by GO on cytosol at the lowest concentrations, avoiding the damage on proteins (lower PC levels), but not on membranes (LPO increase). This study revealed that the presence of GO nanosheets, even at the lower levels tested, impaired behavioural, physiological, and biochemical traits in polychaetes, suggesting that the increase of this engineered nanomaterial in the environment can disturb these benthic organisms, affecting the H. diversicolor population. Moreover, given the important role of this group of organisms in coastal and estuarine food webs, the biogeochemical cycle of nutrients, and sediment oxygenation, there is a real possibility for repercussions into the estuarine community.

Polychlorinated biphenyls (PCBs) are a class of persistent organic pollutants (POPs) that have adverse effects on human health. However, the long-term health effects and potential mechanism of neonatal exposure to PCBs are still unclear. In this study, nursing male mice exposed to PCB138 at 0.5, 5, and 50 μg/kg body weight (bw) from postnatal day (PND) 3 to PND 21 exhibited increased serum uric acid levels and liver uric acid synthase activity at 210 days of age. We also found an increased kidney somatic index in the 50 μg/kg group and kidney fibrosis in the 5 and 50 μg/kg groups. Mechanistically, PCB138 induced mitochondrial dysfunction and endoplasmic reticulum (ER) stress, which might have led to inflammatory responses, such as activation of the NF-κB (nuclear factor kappa-B) and NLRP3 (NOD-like receptor protein 3) pathways. The inflammatory response might regulate renal fibrosis and hypertrophy. In summary, this study reports a long-term effect of neonatal PCB exposure on uric acid metabolism and secondary nephrotoxicity and clarifies the underlying mechanism. Our work also indicates that early life pollutant exposure may be an important cause of diseases later in life.

Exposure to tobacco smoke during pregnancy has been associated with a series of adverse reproductive outcomes; however, the underlying molecular mechanisms are not well-established. We conducted an untargeted metabolome-wide association study to identify the metabolic perturbations and molecular mechanisms underlying the association between cotinine, a widely used biomarker of tobacco exposure, and adverse birth outcomes. We collected early and late pregnancy urine samples for cotinine measurement and serum samples for high-resolution metabolomics (HRM) profiling from 105 pregnant women from the Atlanta African American Maternal-Child cohort (2014–2016). Maternal metabolome perturbations mediating prenatal tobacco smoke exposure and adverse birth outcomes were assessed by an untargeted HRM workflow using generalized linear models, followed by pathway enrichment analysis and chemical annotation, with a meet-in-the-middle approach. The median maternal urinary cotinine concentrations were 5.93 μg/g creatinine and 3.69 μg/g creatinine in early and late pregnancy, respectively. In total, 16,481 and 13,043 metabolic features were identified in serum samples at each visit from positive and negative electrospray ionization modes, respectively. Twelve metabolic pathways were found to be associated with both cotinine concentrations and adverse birth outcomes during early and late pregnancy, including tryptophan, histidine, urea cycle, arginine, and proline metabolism. We confirmed 47 metabolites associated with cotinine levels, preterm birth, and shorter gestational age, including glutamate, serine, choline, and taurine, which are closely involved in endogenous inflammation, vascular reactivity, and lipid peroxidation processes. The metabolic perturbations associated with cotinine levels were related to inflammation, oxidative stress, placental vascularization, and insulin action, which could contribute to shorter gestations. The findings will support the further understanding of potential internal responses in association with tobacco smoke exposures, especially among African American women who are disproportionately exposed to high tobacco smoke and experience higher rates of adverse birth outcomes.

Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans and animals. In adults, thyroid hormones (THs) are regulated by the hypothalamic-pituitary-thyroid (HPT) axis, but also by organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore disrupt the TH system at various locations and through different mechanisms. To start addressing this, we exposed adult male rats to 3 mg PFOS/kg/day for 7 days and analysed effects on multiple organs and pathways simultaneously by transcriptomics. This included four primary organs involved in TH regulation, namely hypothalamus, pituitary, thyroid, and liver. To investigate a potential role of the gut microbiota in thyroid hormone regulation, two additional groups of animals were dosed with the antibiotic vancomycin (8 mg/kg/day), either with or without PFOS. PFOS exposure decreased thyroxine (T4) and triiodothyronine (T3) without affecting thyroid stimulating hormone (TSH), resembling a state of hypothyroxinemia. PFOS exposure resulted in 50 differentially expressed genes (DEGs) in the hypothalamus, 68 DEGs in the pituitary, 71 DEGs in the thyroid, and 181 DEGs in the liver. A concomitant compromised gut microbiota did not significantly change effects of PFOS exposure. Organ-specific DEGs did not align with TH regulating genes; however, genes associated with vesicle transport and neuronal signaling were affected in the hypothalamus, and phase I and phase II metabolism in the liver. This suggests that a decrease in systemic TH levels may activate the expression of factors altering trafficking, metabolism and excretion of TH. At the transcriptional level, little evidence suggests that the pituitary or thyroid gland is involved in PFOS-induced TH system disruption.

The adverse effects of plastic waste and nanoplastics on the water environment have become a focus of global attention in recent years. In the present study, using adult Chinese mitten crabs (Eriocheir sinensis) as an animal model, the bioaccumulation and the in vivo and in vitro toxicity of polystyrene nanoplastics (PS NPs), alone or in combination with the bacteria, were investigated. This study aimed to investigate the effects of PS NPs on apoptosis and glucose metabolism in Chinese mitten crabs, and whether PS NPs could synergistically affect the antibacterial immunity of crabs. We observed that NPs were endocytosed by hemocytes, which are immune cells in crustaceans and are involved in innate immunity. The RNA sequencing data showed that after hemocytes endocytosed NPs, apoptosis and glucose metabolism-related gene expression was significantly induced, resulting in abnormal cell apoptosis and a glucose metabolism disorder. In addition, exposure to NPs resulted in changes in the antimicrobial immunity of crabs, including changes in antimicrobial peptide expression, survival, and bacterial clearance. In summary, NPs could be endocytosed by crab hemocytes, which adversely affected the cell apoptosis, glucose metabolism, and antibacterial immunity of Eriocheir sinensis. This study revealed the effects of NPs on crab immunity and lays the foundation for further exploration of the synergistic effect of NPs and bacteria.

Steroid estrogens have been detected in oceans, rivers, lakes, groundwaters, soils, and even urban water supply systems, thereby inevitably imposing serious impacts on human health and ecological safety. Indeed, many estrogen-degrading bacterial strains and degradation pathways have been reported, with the 4,5-seco pathway being particularly important. However, few studies have evaluated the use of the 4,5-seco pathway by actinomycetes to degrade 17β-estradiol (E2). In this study, 5 genes involved in E2 degradation were identified in the Rhodococcus equi DSSKP-R-001 (R-001) genome and then heterologously expressed to confirm their functions. The transformation of E2 with hsd17b14 reached 63.7% within 30 h, resulting in transformation into estrone (E1). Furthermore, we found that At1g12200-encoded flavin-binding monooxygenase (FMOAₜ₁g₁₂₂₀₀) can transform E1 at a rate of 51.6% within 30 h and can transform E1 into 4-hydroxyestrone (4-OH E1). In addition, catA and hsaC genes were identified to further transform 4-OH E1 at a rate of 97–99%, and this reaction was accomplished by C–C cleavage at the C4 position of the A ring of 4-OH E1. This study represents the first report on the roles of these genes in estrogen degradation and provides new insights into the mechanisms of microbial estrogen metabolism and a better understanding of E2 degradation via the 4,5-seco pathway by actinomycetes.

The presence of contaminants of emerging concern in the aquatic environment directly impacts water-living organisms and can alter their living functions. These compounds are often metabolized and excreted, but they can also be accumulated and spread through the food chain. The metabolized contaminants can also lead to the formation of new compounds with unknown toxicity and bioaccumulation potential. In this work, we have studied the occurrence, bioconcentration, and biotransformation of CECs in glass eels (Anguilla anguilla) using UHPLC-HRMS. To select the target CECs, we first carried out an environmental risk assessment of the WWTP effluent that releases directly into the Adour estuary (Bayonne, Basque Country, France). The risk quotients of every detected contaminant were calculated and three ecotoxicologically relevant contaminants were chosen to perform the exposure experiment: propranolol, diazepam, and irbesartan. An experiment of 14 days consisting of 7 days of exposure and 7 days of depuration was carried out to measure the bioconcentration of the chosen compounds. The quantitative results of the concentrations in glass eel showed that diazepam and irbesartan reached BCF ≈10 on day 7, but both compounds were eliminated after 7 days of depuration. On the other hand, propranolol's concentration remains constant all along with the experiment, and its presence can be detected even in the non-exposed control group, which might suggest environmental contamination. Two additional suspect screening strategies were used to identify metabolization products of the target compounds and other xenobiotics already present in wild glass eels. Only one metabolite was identified, nordiazepam, a well-known diazepam metabolite, probably due to the low metabolic rate of glass eels at this stage. The xenobiotic screening confirmed the presence of more xenobiotics in wild glass eels, prominent among them, the pharmaceuticals exemestane, primidone, iloprost, and norethandrolone.

The link between zinc exposure and glucose metabolism or the development of type 2 diabetes (T2D) is controversial, and underlying mechanisms are unclear. This study aimed to explore the associations of zinc exposure with glucose-insulin homeostasis traits and the long-term effects of zinc on the development of T2D, and further to estimate the potential roles of inflammation and oxidative damage in such relationships. We investigated 3890 urban adults from the Wuhan-Zhuhai cohort, and followed up every three years. Mixed linear model was applied to estimate dose-response associations between urinary zinc and glycemia traits [fasting plasma insulin (FPI), fasting plasma glucose (FPG), insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR), and β-cell dysfunction (homeostasis model assessment of β-cell function, HOMA-B)], as well as zinc and biomarkers for systemic inflammation (C-reactive protein) and oxidative damage (8-isoprostane and 8-hydroxy-2′-deoxyguanosine). Logistic regression model and Cox regression model were conducted to evaluate the relationships between urinary zinc and prevalence and incidence of T2D, respectively. We further performed mediation analysis to assess the roles of inflammation and oxidative damage biomarkers in above associations. At baseline, we observed significant dose-response relationships of elevated urinary zinc with increased FPI, FPG, HOMA-IR, and T2D prevalence and decreased HOMA-B, and such associations could be strengthened by increased C-reactive protein, 8-isoprostane, and 8-hydroxy-2′-deoxyguanosine. Elevated C-reactive protein significantly mediated 9.09% and 17.67% of the zinc-related FPG and HOMA-IR increments, respectively. In longitudinal analysis, a significantly positive association between urinary zinc and T2D incidence was observed among subjects with persistent high urinary zinc levels when compared with those with persistent low zinc levels. Our results suggested that high levels of zinc exposure adversely affected on glucose-insulin homeostasis and further contributed to increased risk of T2D cross-sectionally and longitudinally. Moreover, inflammatory response might play an important role in zinc-related glucose metabolic disorder.

The decay of algal biomass and aquatic plants in freshwater lakes leads to the overproduction of autochthonous organic matter (OM) and the exhaustion of dissolved oxygen, impacting the microbial community and subsequent biodegradation of emerging contaminants in sediment. This study explored how the microbial processing of aquatic plant- and algal-derived OM (POM and AOM) mediates 17α-ethinylestradiol (EE2) biodegradation in the anoxic sediments of Lake Taihu in China. In four months of microcosm incubations, the increased concentrations of protein-like substances in AOM and POM exhibited temporary activation on microbial metabolic enzyme activity (fluorescein diacetate hydrolase and dehydrogenase) and significantly promoted the carbon mineralization with iron reduction (P < 0.001). These in turn increased the EE2 biodegradation efficiency to 77–90 ng g⁻¹ in the anoxic sediment. However, a higher EE2 biodegradation of 109 ng g⁻¹ was achieved with the humic acid augmentation containing more quinone-like compounds, showing a weaker substrate-priming effect but accelerated redox cycling of iron and organic substrates in the later period of incubation. The microbial analysis further revealed that the quinone-like compounds in OM were more closely associated with microbial electron transfer and strengthened their interspecies syntrophic cooperation favorable to contaminant biodegradation, even though the connective members exposed to protein-like components upregulated more functional genes related to organic carbon and xenobiotics metabolism and biodegradation. Our findings will help predict the fate of estrogens in various sedimentary environments under increasing eutrophication and further climate change scenarios.

Aquatic natural colloids are closely related to the environmental behavior of pollutants, which may affect their bioavailability in aquatic organisms. This study explored the potential mechanisms of the natural colloids at environmentally relevant concentrations affecting the bioaccumulation process of benzophenone-3 (BP3) in zebrafish (Danio rerio). The results of kinetic model fitting showed that the natural colloids decreased the uptake and loss rate of BP3 by zebrafish but prolonged the time to reach the cumulative equilibrium, eventually resulting in a higher cumulative concentration in zebrafish. According to the tissue concentration at equilibrium and the results of toxicokinetic analysis, the presence of high molecular colloids could enhance the bioaccumulation of freely dissolved BP3 due to its high desorption rate with BP3 in the intestines of fish, increasing the freely dissolved BP3 concentrations to which zebrafish were exposed. Both natural colloids and BP3 could enhance the cell permeability of zebrafish, which allowed colloid-bound BP3 to directly enter the fish and accumulate in its muscle. Besides, although both natural colloids and BP3 could cause the metabolic disorders in adult zebrafish, they affected the physiological and biochemical activities of zebrafish through different pathways. The disturbance of glutathione metabolism in zebrafish induced by natural colloids may be the reason for the diminished ability of zebrafish to clear and transform BP3 in the mixture system. The carrier effect of natural colloids and reduced clearance ability of zebrafish eventually increased the bioaccumulation of BP3 in zebrafish. This study highlights the significance of natural colloids at environmentally relevant concentrations on the biological effects of emerging contaminants in actual waters, however, natural colloids are always ignored in most field investigation of pollutants, which would ultimately lead to an underestimation of the true ecological risk of pollutants.