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.

Globally, amphibian species are experiencing dramatic population declines, and many face the risk of imminent extinction. Endocrine-disrupting chemicals (EDCs) have been recognised as an underappreciated factor contributing to global amphibian declines. In this regard, the use of hormonal growth promotants in the livestock industry provides a direct pathway for EDCs to enter the environment—including the potent anabolic steroid 17β-trenbolone. Emerging evidence suggests that 17β-trenbolone can impact traits related to metabolism, somatic growth, and behaviour in non-target species. However, far less is known about possible effects of 17β-trenbolone on anuran species, particularly during early life stages. Accordingly, in the present study we investigated the effects of 28-day exposure to 17β-trenbolone (mean measured concentrations: 10 and 66 ng/L) on body size, body condition, metabolic rate, and anxiety-related behaviour of tadpoles (Limnodynastes tasmaniensis). Specifically, we measured rates of O₂ consumption of individual tadpoles as a proxy for metabolic rate and quantified their swimming activity and their time spent in the upper half of the water column as indicators of anxiety-related behaviour. Counter to our predictions based on effects observed in other taxa, we detected no effect of 17β-trenbolone on body size, metabolic rate, or behaviour of tadpoles; although, we did detect a subtle, but statistically significant decrease in body condition at the highest 17β-trenbolone concentration. We hypothesise that 17β-trenbolone may induce taxa-specific effects on metabolic function, growth, and anxiety-related behaviour, with anurans being less sensitive to disruption than fish, and encourage further cross-taxa investigation to test this hypothesis.

The extensive use of nano-TiO₂ has caused concerns regarding their potential environmental risks. However, the stress responses and self-recovery potential of nitrogen removal and greenhouse gas N₂O emissions after long-term nano-TiO₂ exposure have seldom been addressed yet. This study explored the long-term effects of nano-TiO₂ on biological nitrogen transformations in a sequencing batch reactor at four levels (1, 10, 25, and 50 mg/L), and the reactor's self-recovery potential was assessed. The results showed that nano-TiO₂ exhibited a dose-dependent inhibitory effect on the removal efficiencies of ammonia nitrogen and total nitrogen, whereas N₂O emissions unexpectedly increased. The promoted N₂O emissions were probably due to the inhibition of denitrification processes, including the reduction of the denitrifying-related N₂O reductase activity and the abundance of the denitrifying bacteria Flavobacterium. The inhibition of carbon source metabolism, the inefficient electron transfer efficiency, and the electronic competition between the denitrifying enzymes would be in charge of the deterioration of denitrification performance. After the withdrawal of nano-TiO₂ from the influent, the nitrogen transformation efficiencies and the N₂O emissions of activated sludge recovered entirely within 30 days, possibly attributed to the insensitive bacteria survival and the microbial community diversity. Overall, this study will promote the current understanding of the stress responses and the self-recovery potential of BNR systems to nanoparticle exposure.

Ambient air pollutants are well-known risk factors for childhood asthma and asthma exacerbation. It is unknown whether different air pollutants individually or jointly affect pathophysiological mechanisms of asthma. In this study, we aim to integrate transcriptome and untargeted metabolome to identify dysregulated genetic and metabolic pathways that are associated with exposures to a mixture of ambient and traffic-related air pollutants among adults with asthma history. In this cross-sectional study, 102 young adults with childhood asthma history were enrolled from southern California in 2012. Whole blood transcriptome was measured with 20,869 expression signatures, and serum untargeted metabolomics including 937 metabolites were analyzed by Metabolon, Inc. Participants’ exposures to regional air pollutants (NO₂, O₃, PM₁₀, PM₂.₅) and near-roadway air pollutants averaged at one month and one year before study visit were estimated based on residential addresses. xMWAS network analysis and joint-pathway analysis were performed to identify subnetworks and genetic and metabolic pathways that were associated with exposure to air pollutants adjusted for socio-characteristic covariates. Network analysis found that exposures to air pollutants mixture were connected to 357 gene markers and 92 metabolites. One-year and one-month averaged PM₂.₅ and NO₂ were associated with several amino acids related to serine, glycine, and beta-alanine metabolism. Lower serum levels of carnosine and aspartate, which are involved in the beta-alanine metabolic pathway, as well as choline were also associated with worse asthma control (p < 0.05). One-year and one-month averaged PM₁₀ and one-month averaged O₃ were associated with higher gene expression levels of HSPA5, LGMN, CTSL and HLA-DPB1, which are involved in antigen processing and presentation. These results indicate that exposures to various air pollutants are associated with altered genetic and metabolic pathways that affect anti-oxidative capacity and immune response and can potentially contribute to asthma-related pathophysiology.

Cadmium (Cd) is a potentially hazardous element with substantial biological toxicity, adversely affecting plant growth and physiological metabolism. Therefore, it is necessary to explore practical and environment-friendly approaches to reduce toxicity. Jasmonic acid (JA) is an endogenous growth regulator which helps plants defend against biological and abiotic stresses. To determine how JA help relieve Cd toxicity in rice, both laboratory and field experiments were implemented. In the seedling stage, the role of JA in mediating rice Cd tolerance was investigated via a fluorescent probe in vivo localization, Fourier Transform Infrared Spectroscopy (FTIR), and colorimetry. At the mature growth stage of rice, field experiments were implemented to research the effects of JA on the Cd uptake and translocation in rice. In the seedling stage of rice, we found that JA application increased the cell wall compartmentalization of Cd by promoting the Cd combination on chelated-soluble pectin of rice roots and inhibited Cd movement into protoplasts, thereby reducing the Cd content in the roots by 30.5% and in the shoots by 53.3%, respectively. Application of JA reduced H₂O₂ content and helped relieve Cd-induced peroxidation damage of membrane lipid by increasing the level of catalase (CAT), peroxidase (POD), ascorbate peroxidase (APX), and glutathione (GSH), but had no significant effect on the superoxide dismutase (SOD) activity. Additionally, field experiments showed that foliar spraying of JA inhibited rice Cd transport from the stalk and root to the grain and reduced Cd concentration in grain by 29.7% in the high-Cd fields and 28.0% in the low-Cd fields. These results improve our understanding of how JA contributes to resistance against Cd toxicity in rice plants and reduces the accumulation of Cd in rice kernels.

Arsenic (As) and cadmium (Cd), two major carcinogenic heavy metals, enters into human food chain by the consumption of rice or rice-based food products. Both As and Cd disturb plant-nutrient homeostasis and hence, reduces plant growth and crop productivity. In the present study, As/Cd modulated responses were studied in non-basmati (IR-64) and basmati (PB-1) rice varieties, at physiological, biochemical and transcriptional levels. At the seedling stage, PB-1 was found more sensitive than IR-64, in terms of root biomass; however, their shoot phenotype was comparable under As and Cd stress conditions. The ionomic data revealed significant nutrient deficiencies in As/Cd treated-roots. The principal component analysis identified NH₄⁺ as As-associated key macronutrient; while, NH₄⁺/NO₃⁻ and K⁺ was majorly associated with Cd mediated response, in both IR-64 and PB-1. Using a panel of 21 transporter gene expression, the extent of nutritional deficiency was ranked in the order of PB-1(As)<IR-64(As)<PB-1(Cd)<IR-64(Cd). A feed-forward model is proposed to explain nutrient deficiency induced de-regulation of gene expression, as observed under Cd-treated IR-64 plants, which was also validated at the level of sulphur metabolism related enzymes. Using urea supplementation, as nitrogen-fertilizer, significant mitigation was observed under As stress, as indicated by 1.018- and 0.794-fold increase in shoot biomass in IR-64 and PB-1, respectively compared to that of control. However, no significant amelioration was observed in response to supplementation of urea under Cd or potassium under As/Cd stress conditions. Thus, the study pinpointed the relative significance of various macronutrients in regulating As- and Cd-tolerance and will help in designing suitable strategies for mitigating As and/or Cd stress conditions.

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.

Research on per- and polyfluoroalkyl substances (PFAS) in freshwater ecosystems has focused primarily on legacy compounds and little is still known on the presence of emerging PFAS. Here, we investigated the occurrence of 60 anionic, zwitterionic, and cationic PFAS in a food web of the St. Lawrence River (Quebec, Canada) near a major metropolitan area. Water, sediments, aquatic vegetation, invertebrates, and 14 fish species were targeted for analysis. Levels of perfluorobutanoic acid (PFBA) in river water exceeded those of perfluorooctanoic acid (PFOA) or perfluorooctane sulfonate (PFOS), and a zwitterionic betaine was observed for the first time in the St. Lawrence River. The highest mean PFAS concentrations were observed for the benthopelagic top predator Smallmouth bass (Micropterus dolomieu, Σ₆₀PFAS ∼ 92 ± 34 ng/g wet weight whole-body) and the lowest for aquatic plants (0.52–2.3 ng/g). Up to 33 PFAS were detected in biotic samples, with frequent occurrences of emerging PFAS such as perfluorobutane sulfonamide (FBSA) and perfluoroethyl cyclohexane sulfonate (PFECHS), while targeted ether-PFAS all remained undetected. PFOS and long-chain perfluorocarboxylates (C10–C13 PFCAs) dominated the contamination profiles in biota except for insects where PFBA was predominant. Gammarids, molluscs, and insects also had frequent detections of PFOA and fluorotelomer sulfonates, an important distinction with fish and presumably due to different metabolism. Based on bioaccumulation factors >5000 and trophic magnification factors >1, long-chain (C10–C13) PFCAs, PFOS, perfluorodecane sulfonate, and perfluorooctane sulfonamide qualified as very bioaccumulative and biomagnifying. Newly monitored PFAS such as FBSA and PFECHS were biomagnified but moderately bioaccumulative, while PFOA was biodiluted.