International audience | Insects play many important roles in nature due to their diversity, ecological role, and impact on agriculture or human health. They are directly influenced by environmental changes and in particular anthropic activities that constitute an important driver of change in the environmental characteristics. Insects face numerous anthropogenic stressors and have evolved various detoxication mechanisms to survive and/or resist to these compounds. Recent studies highligted the pressure exerted by xenobiotics on insect life-cycle and the important role of insect-associated bacterial microbiota in the insect responses to environmental changes. Stressor exposure can have various impacts on the composition and structure of insect microbiota that in turn may influence insect biology. Moreover, bacterial communities associated with insects can be directly or indirectly involved in detoxification processes with the selection of certain microorganisms capable of degrading xenobiotics. Further studies are needed to assess the role of insect-associated microbiota as key contributor to the xenobiotic metabolism and thus as a driver for insect adaptation to polluted habitats.

[Departement_IRSTEA]Ecotechnologies [TR1_IRSTEA]TED [Axe_IRSTEA]TED-EPURE | International audience | Xenobiotics such as pesticides and pharmaceuticals are an increasingly large problem in aquatic environments. A fixed-bed adsorption filter, used as tertiary stage of sewage treatment, could be a solution to decrease xenobiotics concentrations in wastewater treatment plants (WWTPs) effluent. The adsorption efficiency of two mineral adsorbent materials (expanded clay (EC) and zeolite (ZE)), both seen as a possible alternative to activated carbon (AC), was evaluated in batch tests. Experiments involving secondary treated domestic wastewater spiked with a cocktail of ten xenobiotics (eight pharmaceuticals and two pesticides) known to be poorly eliminated in conventional biological process were carried out. Removal efficiencies and partitions coefficientswere calculated for two levels of initial xenobiotic concentration, i.e, concentrations lower to 10 microg/L and concentrations ranged from 100 to 1,000 microg/L. While AC was the most efficient adsorbent material, both alternative adsorbent materials showed good adsorption efficiencies for all ten xenobiotics (from 50 to 100 % depending on the xenobiotic/adsorbent material pair). For all the targeted xenobiotics, at lower concentrations, EC presented the best adsorption potential with higher partition coefficients, confirming the results in terms of removal efficiencies. Nevertheless, Zeolite presents virtually the same adsorption potential for both high and low xenobiotics concentrations to be treated. According to this first batch investigation, ZE and EC could be used as alternative absorbent materials to AC in WWTP.

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 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.

Perfluorooctane sulfonate (PFOS) is one of the most widely used and distributed perfluorinated compounds proven to cause adverse health outcomes. Datasets of ecotoxico-genomics and proteomics have given greater insights for PFOS toxicological effect. However, the molecular mechanisms of hepatotoxicity of PFOS on post-translational modifications (PTMs) regulation, which is most relevant for regulating the activity of proteins, are not well elucidated. Protein glycosylation is one of the most ubiquitous PTMs associated with diverse cellular functions, which are critical towards the understanding of the multiple biological processes and toxic mechanisms exposed to PFOS. Here, we exploit the multilayered glycoproteomics to quantify the global protein expression levels, glycosylation sites, and glycoproteins in PFOS exposure and wild-type mouse livers. The identified 2439 proteins, 1292 glycosites, and 799 glycoproteins were displayed complex heterogeneity in PFOS exposure mouse livers. Quantification results reveal that 241 dysregulated proteins (fold change ≥ 2, p < 0.05) in PFOS exposure mouse livers were involved in the lipid and xenobiotic metabolism. While, 16 overexpressed glycoproteins were exclusively related to neutrophil degranulation, cellular responses to stress, protein processing in endoplasmic reticulum (ER). Moreover, the interactome and functional network analysis identified HP and HSP90AA1 as the potential glycoprotein biomarkers. These results provide unique insights into a deep understanding of the mechanisms of PFOS induced hepatotoxicity and liver disease. Our platform of multilayered glycoproteomics can be adapted to diverse ecotoxicological research.

Fomesafen (FSA) is widely used in soybean fields for weed control. However, the persisting characteristics of FSA in the agricultural soil or water may become a hidden danger causing environmental pollution and phytotoxicity to succession crops. In this study, the growth and physiological responses of rice to FSA were investigated. It was found that the growth of rice seedlings was obviously inhibited by FSA exposure especially at over 0.1 mg L⁻¹. To gain an insight into the molecular mechanisms for the potential ecotoxicology, four libraries of rice roots and shoots exposed to FSA were created and subjected to the global RNA-sequencing (RNA-Seq) combined with HRLC-Q-TOF-MS/MS analytical technologies to comprehensively characterize the biochemical processes and catalytic reactions involved in FSA metabolism in rice. Compared with those without FSA, 499 and 450 up-regulated genes in roots and shoots with FSA were detected. Many of them were closely correlated with the tolerance to environmental stress, detoxification of xenobiotics and molecular metabolism process including cytochrome P450, glutathione S-transferases and acetyltransferase. A total of eight metabolites and fourteen conjugates in the reactive pathways of hydrolysis, substitution, reduction, methylation, glycosylation, acetylation, and malonylation were characterized by HRLC-Q-TOF-MS/MS. The relationship between the metabolized derivatives of FSA and enhanced expression the corresponding enzymatic regulators was established. This study will help understand the mechanisms and pathways of FSA metabolism and inspire the further research on FSA degradation in the paddy crops and environmental or health risks.

Sulfur, an essential macronutrient, plays important roles in plant development and stress mitigation. Sulfur deficiency, a common problem in agricultural soils, may disturb plant stress resistance and xenobiotic detoxification. In the present study, the function and mechanism of limited sulfur nutrition on the residues and phtotoxicity of imidacloprid were investigated in lettuce plants. Sulfur deficiency significantly increased imidacloprid accumulation in lettuce tissues, exacerbated imidacloprid biological toxicity by enhancing the accumulation of toxic metabolites, like imidacloprid-olefin. Simultaneously, imidacloprid-induced detoxification enzymes including cytochromes P450, glutathione S-transferases (GSTs) and glycosyltransferases were inhibited under limited sulfur supply. On the other hand, sulfur deficiency further enhanced the generation of reactive oxygen species and exacerbated lipid peroxidation in lettuce tissues. Sulfur deficiency mainly reduced the abundance of thiol groups, which are essential redox modulators as well as xenobiotic conjugators, and significantly inhibited GSTs expression. These results clearly suggested that sulfur deficiency inhibited the synthesis of sulfur-containing compounds, leading to increased accumulation of pesticide residues and toxic metabolites as well as reduced detoxification capacity, consequently leading to oxidative damage to plants. Therefore, moderate sulfur supply in regions where neonicotinoid insecticides are intensively and indiscriminately used may be an efficient strategy to reduce pesticide residues and the potential risk to ecosystem.

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.

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.