Tebuconazole is a broad-spectrum triazole fungicide that has been extensively applied in agriculture, but its toxicity on soil ecology remains unknown after repeated introduction to soil. This study investigated the degradation of tebuconazole and the changes in soil microbial community composition and functional diversity as well as network complexity in soil repeatedly treated with tebuconazole. Tebuconazole degraded slowly as the degradation half-life initially increased and then decreased during the four repeated treatments. High concentration of tebuconazole treatment significantly delayed the degradation of tebuconazole. The soil microbial functional diversity in tebuconazole-treated soils showed an inhibition-recovery-stimulation trend with increasing treatment frequency, which was related to the increased degradation rates of tebuconazole. Tebuconazole significantly decreased soil microbial biomass and bacterial community diversity, and this decreasing trend became more pronounced with increasing treatment frequency and concentration. Moreover, tebuconazole significantly decreased soil bacterial community network complexity, particularly at high concentration of tebuconazole treatment. Notably, four bacterial genera, Methylobacterium, Burkholderia, Hyphomicrobium, and Dermacoccus, were identified as the potential tebuconazole-degrading bacteria, with the relative abundances in the tebuconazole treatment significantly increasing by 42.1–34687.1% compared to the control. High concentration of tebuconazole treatment delayed increases in the relative abundances of Methylobacterium but promoted those of Burkholderia, Hyphomicrobium and Dermacoccus. Additionally, repeated tebuconazole treatments improved only four metabolic pathways, cell motility, membrane transport, environmental information processing, and xenobiotics biodegradation and metabolism, which were associated with the degradation of tebuconazole. The above results indicated that repeated tebuconazole treatments resulted in the significant accumulation of residues and long-term negative effects on soil ecology, and also emphasized the potential roles of dominant indigenous microbial bacteria in the degradation of tebuconazole.

Cresyl diphenyl phosphate (CDP), as a kind of aryl substituted organophosphate esters (OPEs), is commonly used as emerging flame retardants and plasticizers detected in environmental media. Due to the accumulation of CDP in organisms, it is very important to discover the toxicological mechanism and metabolic process of CDP. Hence, liver microsomes of crucian carps (Carassius carassius) were prepared for in vitro metabolism kinetics assay to estimate metabolism rates of CDP. After 140 min incubation, the depletion of CDP accounted for 58.1%–77.1% (expect 0.5 and 2 μM) of the administrated concentrations. The depletion rates were best fitted to the Michaelis-Menten model (R² = 0.995), where maximum velocity (Vₘₐₓ) and Michaelis-Menten constant (Kₘ) were 12,700 ± 2120 pmol min⁻¹·mg⁻¹ protein and 1030 ± 212 μM, respectively. Moreover, the in vitro hepatic clearance (CLᵢₙₜ) of CDP was 12.3 μL min⁻¹·mg⁻¹ protein. Log Kₒw and bioconcentration factor (BCF) of aryl-OPEs were both higher than those of alkyl- and chlorinated-OPEs, indicating that CDP may easily accumulate in aquatic organisms. The results made clear that the metabolism rate of CDP was greater than those of other OPEs detected in liver microsomes in previous research. This paper was first of its kind to comprehensively investigate the in vitro metabolic kinetics of CDP in fish liver microsomes. The present study might provide useful information to understand the environmental fate and metabolic processes of these kinds of substances, and also provide a theoretical basis for the ecological risk assessment of emerging contaminants.

6:2 Cl-PFESA is a polyfluoroalkyl ether with high environmental persistence that has been confirmed to have significant adverse effects on animals. In this study, 6-week-old female C57BL/6 mice were exposed to 0, 1, 3 and 10 μg/L 6:2 Cl-PFESA for 10 weeks to estimate the hepatotoxicity of 6:2 Cl-PFESA and explore its underlying molecular mechanism. The results indicated that 6:2 Cl-PFESA preferentially bioaccumulated in the liver and induced hepatic cytoplasmic vacuolation and hepatomegaly in mice. In addition, serum metabolic profiling showed that 6:2 Cl-PFESA exposure caused an abnormal increase in amino acids and an abnormal decrease in acyl-carnitine, which interfered with fatty acid transport and increased the risk of metabolic diseases. Further experiments showed that 6:2 Cl-PFESA formed more hydrogen bonds with PPAR-γ than PFOS, Rosi and GW9662, and the binding affinity of 6:2 Cl-PFESA toward PPAR-γ was the highest among the ligands. 6:2 Cl-PFESA promoted the differentiation of 3T3-L1 cells by increasing PPAR-γ expression. Therefore, our results showed that 6:2 Cl-PFESA has the potential to induce liver damage and dysfunction in female mice, and this effect was achieved through PPAR-γ. This study is the first to reveal the hepatic toxicity of 6:2 Cl-PFESA in female mammals and provides new insights for subsequent in-depth research.

Pharmaceutical pollution is now recognised as a major emerging agent of global change. Increasingly, pharmaceutical pollutants are documented to disrupt ecologically important physiological and behavioural traits in exposed wildlife. However, little is known about potential impacts of pharmaceutical exposure on among-individual variation in these traits, despite phenotypic diversity being critical for population resilience to environmental change. Furthermore, although wildlife commonly experience multiple stressors contemporaneously, potential interactive effects between pharmaceuticals and biological stressors—such as predation threat—remain poorly understood. To redress this, we investigated the impacts of long-term exposure to the pervasive pharmaceutical pollutant fluoxetine (Prozac®) on among-individual variation in metabolic and behavioural traits, and the combined impacts of fluoxetine exposure and predation threat on mean metabolic and behavioural traits in a freshwater fish, the guppy (Poecilia reticulata). Using a mesocosm system, guppy populations were exposed for 15 months to one of two field-realistic levels of fluoxetine (nominal concentrations: 30 and 300 ng/L) or a solvent control. Fish from these populations were then tested for metabolic rate (oxygen uptake) and behaviour (activity), both before and after experiencing one of three levels of a predation treatment: an empty tank, a non-predatory fish (Melanotaenia splendida) or a predatory fish (Leiopotherapon unicolor). Guppies from both fluoxetine treatments had ∼70% lower among-individual variation in their activity levels, compared to unexposed fish. Similarly, fluoxetine exposure at the higher dosage was associated with a significant (26%) reduction in individual-level variation in oxygen uptake relative to unexposed fish. In addition, mean baseline metabolic rate was disrupted in low-fluoxetine exposed fish, although mean metabolic and behavioural responses to predation threat were not affected. Overall, our study demonstrates that long-term exposure to a pervasive pharmaceutical pollutant alters ecologically relevant traits in fish and erodes among-individual variability, which may be detrimental to the stability of contaminated populations globally.

The molecular mechanism of evaluating 17β-estradiol (E₂)-induced toxicity in female Daphnia magna has not been determined. In this study, the transcriptome of D. magna was analyzed after exposure to three different concentrations (0, 10, and 100 ng L⁻¹) of E₂ at 3, 6, and 12 h. The results showed 351–17,221 significantly up-regulated and 505–10,282 significantly down-regulated genes (P < 0.05). Overall, the selected largest 10,282 (10 ng L⁻¹vs control at 12 h) down-regulated and 17,221 (100 vs 10 ng L⁻¹) up-regulated genes were identified; following annotation, pathways in cancer and RNA transport were found to be enriched according to the interaction network. Among all completed comparisons, KEGG pathways related to the immune system, cancer, disease infection, and active compound metabolism were identified by short time series expression miner analysis. A different set of genes fluctuated in a “U”-shaped pattern over time and at different concentrations of E₂, whereas some genes associated with disintoxication showed a reverse “U”-shaped response as E₂ administration was increased. These results suggest that E₂ exposure caused transcriptional changes in the immune system, disintoxication, disease prevention, and the protein degradation pathway.

Approximately 3 billion people world-wide are exposed to air pollution from biomass burning. Herein, particulate matter (PM) emitted from artisanal cashew nut roasting, an important economic activity worldwide, was investigated. This study focused on: i) chemical characterization of polycyclic aromatic hydrocarbons (PAHs) and oxygenated (oxy-) PAHs; ii) intracellular levels of reactive oxygen species (ROS); iii) genotoxic effects and time- and dose-dependent activation of DNA damage signaling, and iv) differential expression of genes involved in xenobiotic metabolism, inflammation, cell cycle arrest and DNA repair, using A549 lung cells. Among the PAHs, chrysene, benzo[a]pyrene (B[a]P), benzo[b]fluoranthene, and benz[a]anthracene showed the highest concentrations (7.8–10 ng/m³), while benzanthrone and 9,10-anthraquinone were the most abundant oxy-PAHs. Testing of PM extracts was based on B[a]P equivalent doses (B[a]Pₑq). IC₅₀ values for viability were 5.7 and 3.0 nM B[a]Pₑq at 24 h and 48 h, respectively. At these low doses, we observed a time- and dose-dependent increase in intracellular levels of ROS, genotoxicity (DNA strand breaks) and DNA damage signaling (phosphorylation of the protein checkpoint kinase 1 – Chk1). In comparison, effects of B[a]P alone was observed at micromolar range. To our knowledge, no previous study has demonstrated an activation of pChk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro, in lung cells exposed to cashew nut roasting extracts. Sustained induction of expression of several important stress response mediators of xenobiotic metabolism (CYP1A1, CYP1B1), ROS and pro-inflammatory response (IL-8, TNF-α, IL-2, COX2), and DNA damage response (CDKN1A and DDB2) was also identified. In conclusion, our data show high potency of cashew nut roasting PM to induce cellular stress including genotoxicity, and more potently when compared to B[a]P alone. Our study provides new data that will help elucidate the toxic effects of low-levels of PAH mixtures from air PM generated by cashew nut roasting.

In order to examine whether 8:2 FTOH exposure would lead to a contamination risk of perfluoroalkyl and polyfluoroalkyl substances (PFASs) in broiler derived food, the biotransformation, and tissue distribution and accumulation of 8:2 FTOH following oral exposure in male broilers were investigated. The main metabolites of 8:2 FTOH in plasma and six tissues (muscle, liver, kidney, fat, heart, and lungs) identified by LC-Q-TOF were 2-perfluorooctyl ethanoic acid (8:2 FTCA), 8:2 fluorotelomer unsaturated carboxylic acid (8:2 FTUCA), 3-perfluoroheptyl propanoic acid (7:3 FTCA), perfluoropentanoic acid (PFPeA), perfluorooctanoic acid (PFOA), perfluoroheptanoic acid (PFHpA), perfluorohexanoic acid (PFHxA), perfluorononanoic acid (PFNA), 8:2 FTOH glucuronide conjugate, and 8:2 FTOH sulfate conjugate. The tissue distribution and bioaccumulation of 8:2 FTOH and its unconjugated metabolites were determinated by LC-MS/MS. 8:2 FTOH was quickly depleted in plasma and all six tested tissues, while PFOA, PFNA, and 7:3 FTCA showed strong accumulation in blood and all six examined tissues and were eliminated more slowly than the other metabolites. The tissues with the highest accumulation levels for 8:2 FTOH and its metabolites were heart, kidneys and liver, and the tissue with the lowest accumulation levels was muscle. The elimination half-lifes of PFNA in kidney and 7:3 FTCA in lung were longer compared to those of other metabolites in all six determined tissues. Thus, PFNA and 7:3 FTCA can be selected as potential biomonitoring markers after 8:2 FTOH exposure. This study has improved our understanding of 8:2 FTOH biotransformation and tissue bioaccumulation in broilers, which will help us monitor human exposure risk via food derived from broilers polluted by 8:2 FTOH.

Considering the increasing use of Lithium (Li) and the necessity to fulfil this demand, labile Li occurrence in the environment will be enhanced. Thus, additional research is needed regarding the presence of this element in marine environment and its potential toxic impacts towards inhabiting wildlife. The aim of the present study was to evaluate Li toxicity based on the exposure of Mytilus galloprovincialis to this metal, assessing the biochemical changes related with mussels’ metabolism, oxidative stress and neurotoxicity. For this, organisms were exposed to different Li concentrations (100, 250, 750 μg/L) for 28 days. The results obtained clearly demonstrated that Li lead to mussels’ metabolism depression. The present study also revealed that, especially at the highest concentrations, antioxidant and biotransformation enzymes were not activated, leading to the occurrence of lipid peroxidation and loss of redox homeostasis, with increased content in oxidized glutathione in comparison to the reduced form. Furthermore, after 28 days, higher Li exposure concentrations induced neurotoxic effects in mussels, with a decrease in acetylcholinesterase enzyme activity. The responses observed were closely related with Li concentrations in mussels’ tissues, which were more pronounced at higher exposure concentrations. Such results highlight the potential toxic effects of Li to marine species, which may even be higher under predicted climate changes and/or in the presence of other pollutants.

Tris (2-ethylhexyl) phosphate (TEHP) is one of the most commonly used organophosphorus flame retardant (OPFR) analogues and is commonly detected in surface water and sediments. Limited information is available about the metabolic pathway or metabolite formation related to TEHP in fish. In this study, rare minnows (Gobiocyprisrarus) were exposed to TEHP in static water for 30 d to investigate the bioaccumulation and metabolite distribution in the fish muscle, liver, kidney, gill, GI-tract, ovary and testis. Based on the estimated kᵤₚ,ₚₐᵣₑₙₜ and kd,ₚₐᵣₑₙₜ values, the bioconcentration factors (BCFₚₐᵣₑₙₜ) of TEHP in fish tissues were calculated in the order of kidney > ovary ≈ liver ≈ testis > gill ≈ GI-tract > muscle; this finding was consistent with the results of our previous study on other alkyl-substituted OPFRs. In addition, this study identified the metabolic profiles of TEHP in the liver. TEHP was oxidatively metabolized by the fish to a dealkylated metabolite (di 2-ethylhexyl phosphate; DEHP) and hydroxylated TEHP (OH-TEHP). OH-TEHP further underwent extensive phase II metabolism to yield glucuronic acid conjugates. DEHP was mainly distributed in rare minnow in the following order: liver > GI-tract > kidney ≫ other tissues. However, the metabolite showed lower accumulation potential in fish tissues than TEHP, with metabolite parent concentration factors (MPCFs) for DEHP of less than 0.1 in all the investigated tissues. The BCFₚₐᵣₑₙₜ values of TEHP in various fish tissues were only 9.0 × 10⁻³-7.2 × 10⁻⁴ times its estimated tissue-water partition coefficient (Kₜᵢₛₛᵤₑ₋wₐₜₑᵣ) values based on tissue lipid, protein and water contents, which indicated the significance of biotransformation in reducing the bioaccumulation potential of TEHP in fish. The toxicokinetic data in the present study help in understanding the tissue-specific bioaccumulation and metabolism pathways of TEHP in fish and highlight the importance of toxicology research on TEHP metabolites in aquatic organisms.

Arsenic (As) has been recognized as one of the most toxic metalloids present in the surface soil contaminating food chain and posing threat to human life. Sulfur (S) fertilizer is often supplied in paddy soil for rice growth, but its impact on As mobility and related bacteria remains poorly understood. In this study, a pot experiment was set up with two different types of sulfur treatments (element sulfur and Na₂SO₄) to evaluate the effect of sulfur fertilizers on As speciation in porewater, As fractions in soil, As accumulation in rice plants. Besides, rhizosphere bacterial composition and functional genes that might influence As mobility were also studied. The results revealed that the addition of 150 mg/kg Na₂SO₄ decreased As(III) and As(V) concentrations in soil porewater at maturation stage by 77% and 64%, respectively. With the same sulfur content, Na₂SO₄ was more effective than element sulfur. The addition of sulfur fertilizers promoted rice growth and reduced As accumulation in shoots, further reduced As translocation from root to above-ground parts by 39–59%. The addition of sulfur fertilizers had little effect on genes involved in As metabolism. However, the relative abundance of Fe(III) and sulfate reduction related genera increased with the addition of 150 mg/kg Na₂SO₄, consistent with the increase of Fe(III) reducing bacteria Geobacteraceae and sulfate reducing gene dsrA. The phenomenon likely influenced the decrease of As concentrations in soil porewater and rice uptake. The outcomes indicate that promoting Fe- and S- reducing bacteria in the rhizosphere by sulfur fertilizers may be one way to reduce As risk in the soil-rice system.