Dinotefuran is a third-generation neonicotinoid pesticide and is increasingly used in agricultural production, which has adverse effects on nontarget organisms. However, the research on the impact of dinotefuran on nontarget organisms is still limited. Here the toxic effects of dinotefuran on an important economic species and a model lepidopteran insect, Bombyx mori, were investigated. Exposure to different doses of dinotefuran caused physiological disorders or death. Cytochrome P450, glutathione S-transferase, carboxylesterase, and UDP glycosyl-transferase activities were induced in the fat body at early stages after dinotefuran exposure. By contrast, only glutathione S-transferase activity was increased in the midgut. To overcome the lack of sensitivity of the biological assays at the individual organism level, RNA sequencing was performed to measure differential expressions of mRNA from silkworm larvae after dinotefuran exposure. Differential gene expression profiling revealed that various detoxification enzyme genes were significantly increased after dinotefuran exposure, which was consistent with the upregulation of the detoxifying enzyme. The global transcriptional pattern showed that the physiological responses induced by dinotefuran toxicity involved multiple cellular processes, including energy metabolism, oxidative stress, detoxification, and other fundamental physiological processes. Many metabolism processes, such as carbon metabolism, fatty acid biosynthesis, pyruvate metabolism, and the citrate cycle, were partially repressed in the midgut or fat body. Furthermore, dinotefuran significantly activated the MAPK/CREB, CncC/Keap1, PI3K/Akt, and Toll/IMD pathways. The links between physiological, biochemical toxicity and comparative transcriptomic analysis facilitated the systematic understanding of the integrated biological toxicity of dinotefuran. This study provides a holistic view of the toxicity and detoxification metabolism of dinotefuran in silkworm and other organisms.

Bisphenol S is an endocrine disruptor exhibiting metabolic disturbances, especially following perinatal exposures. To date, no data are available on the obesogen effects of BPS in a mutligenerational issue.We investigated obesogen effects of BPS in a multigenerational study by focusing on body weight, adipose tissue and plasma parameters in male and female mice.Pregnant C57BL6/J mice were exposed to BPS (1.5 μg/kg bw/day ie a human equivalent dose of 0.12 μg/kg bw/day) by drinking water from gestational day 0 to post natal day 21. All offsprings were fed with a high fat diet during 15 weeks. Body weight was monitored weekly and fat mass was measured before euthanasia. At euthanasia, blood glucose, insuline, triglyceride, cholesterol and no esterified fatty acid plasma levels were determined and gene expressions in visceral adipose tissue were assessed. F1 males and females were mated to obtain the F2 generation. Likewise, the F2 mice were cross-bred to obtain F3. The same analyses were performed.In F1 BPS induced an overweight in male mice associated to lipolysis gene expressions upregulation. In F1 females, dyslipidemia was observed. In F2, BPS exposure was associated to an increase in body weight, fat and VAT masses in males and females. Several plasma parameters were increased but with a sex related pattern (blood glucose, triglycerides and cholesterol in males and NEFA in females). We observed a down-regulation in mRNA expression of gene involved in lipogenesis and in lipolysis for females but only in the lipogenesis for males. In F3, a decrease in VAT mass and an upregulation of lipogenesis gene expression occurred only in females.BPS perinatal exposure induced sex-dependent obesogen multigenerational effects, the F2 generation being the most impacted. Transgenerational disturbances persisted only in females.

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.

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.

Excess nitrate has been reported to be associated with many adverse effects in humans and experimental animals. However, there is a paucity of information of the effects of nitrate on intestinal microbial community. In this study, the effects of nitrate on development, intestinal microbial community, and metabolites of Bufo gargarizans tadpoles were investigated. B. gargarizans were exposed to control, 5, 20 and 100 mg/L nitrate-nitrogen (NO₃–N) from eggs to Gosner stage 38. Our data showed that the body size of tadpoles significantly decreased in the 20 and 100 mg/L NO₃–N treatment group when compared to control tadpoles. Exposure to 20 and 100 mg/L NO₃–N also caused indistinct cell boundaries and nuclear pyknosis of mucosal epithelial cells in intestine of tadpoles. In addition, exposure to NO₃–N significantly altered the intestinal microbiota diversity and structure. The facultative anaerobic Proteobacteria occupy the niche of the obligately anaerobic Bacteroidetes and Fusobacteria under the pressure of NO₃–N exposure. According to the results of functional prediction, NO₃–N exposure affected the fatty acid metabolism pathway and amino acid metabolism pathway. The whole-body fatty acid components were found to be changed after exposure to 100 mg/L NO₃–N. Therefore, we concluded that exposure to 20 and 100 mg/L NO₃–N could induce deficient nutrient absorption in intestine, resulting in malnutrition of B. gargarizans tadpoles. High levels of NO₃–N could also change the intestinal microbial communities, causing dysregulation of fatty acid metabolism and amino acid metabolism in B. gargarizans tadpoles.

Marine fish are considered a source of high quality proteins and fatty acids. However, the consumption of fish may pose a health risk as it may have potentially toxic elements in high concentrations. In this study we quantify the multielemental composition of muscle and fins for three species of commercial marine fish from Brazil: Sphyraena guachancho (Barracuda), Priacantus arenatus (Common bigeye) and Genidens genidens (Guri sea catfish). We then assessed the potential risk of fish consumption by means of a Provisional Hazard Indices. Amongst the elements detected in fish tissue were potentially toxic elements such as Ag, Ba, Cd, Cr and Hg. Concentration differences were species-specific, and affected by the species trophic level, morphological characteristics and feeding habits. Results suggest the higher the trophic level of the fish, the higher the risk of consumption. Caution is recommended for the frequent ingestion of high trophic level fish species in Brazil.

Exposure to ambient particular matters (PM) has been associated with the development of non-alcoholic fatty liver disease (NAFLD), but the underlying mechanism remains unclear. Given that microRNA (miRNA) is recognized as a key regulator of lipid metabolism and a potential mediator of environmental cues, this study aimed to explore the role of miRNA-mRNA regulation underlying abnormal lipid metabolism triggered by PM₂.₅liposoluble extracts. We confirmed that 72-h exposure to liposoluble extracts of PM₂.₅ from Nanjing at 25 μg/cm² induced lipid accumulation in HepG2 cells by promoting uptake of free fatty acids (FFAs). Notably, lipid accumulation induced by PM₂.₅ liposoluble extracts was associated with decreased expression of miR-26a and consequent upregulation of fatty acid translocase (FAT, also known as CD36). Using gain- and loss-of-function assays, we demonstrated that miR-26a negatively regulated CD36 to mediate lipid accumulation in HepG2 cells. We further confirmed that miR-26a directly acted on the 3′ untranslated region (3′UTR) of CD36. Furthermore, overexpression of miR-26a abolished steatosis in HepG2 cells treated with PM₂.₅ liposoluble extracts by suppressing CD36. In addition, we demonstrated that PM₂.₅ liposoluble extracts caused inflammation in HepG2 cells by raising p65 phosphorylation, thereby fuelling the transition from simple non-alcoholic fatty liver to non-alcoholic steatohepatitis. In conclusion, this study demonstrated a novel mechanism by which miR-26a-CD36 pathway mediated lipid accumulation induced by PM₂.₅ liposoluble extracts in hepatocytes. Lipid accumulation and inflammation induced by PM₂.₅ liposoluble extracts implied the potential role of PM₂.₅ in developing NAFLD.

Pacific Ocean trawl samples, stomach contents of laboratory-raised fish as well as fish from the subtropical gyres were analyzed by Raman micro-spectroscopy (RMS) to identify polymer residues and any detectable persistent organic pollutants (POP). The goal was to access specific molecular information at the individual particle level in order to identify polymer debris in the natural environment. The identification process was aided by a laboratory generated automated fluorescence removal algorithm. Pacific Ocean trawl samples of plastic debris associated with fish collection sites were analyzed to determine the types of polymers commonly present. Subsequently, stomach contents of fish from these locations were analyzed for ingested polymer debris. Extraction of polymer debris from fish stomach using KOH versus ultrapure water were evaluated to determine the optimal method of extraction. Pulsed ultrasonic extraction in ultrapure water was determined to be the method of choice for extraction with minimal chemical intrusion. The Pacific Ocean trawl samples yielded primarily polyethylene (PE) and polypropylene (PP) particles >1 mm, PE being the most prevalent type. Additional microplastic residues (1 mm - 10 μm) extracted by filtration, included a polystyrene (PS) particle in addition to PE and PP. Flame retardant, deca-BDE was tentatively identified on some of the PP trawl particles. Polymer residues were also extracted from the stomachs of Atlantic and Pacific Ocean fish. Two types of polymer related debris were identified in the Atlantic Ocean fish: (1) polymer fragments and (2) fragments with combined polymer and fatty acid signatures. In terms of polymer fragments, only PE and PP were detected in the fish stomachs from both locations. A variety of particles were extracted from oceanic fish as potential plastic pieces based on optical examination. However, subsequent RMS examination identified them as various non-plastic fragments, highlighting the importance of chemical analysis in distinguishing between polymer and non-polymer residues.

The gulf of Annaba, the most important touristic and economic coastal zone located in Northeast Algeria, is contaminated by several pollutants from urban, agricultural, harbor and industrial activities. Elevated levels of heavy metals were detected in a locally prevalent edible mollusk Donax trunculus (Bivalvia, Donacidae) widely used as a sentinel species for the assessment of marine pollution. The present work aims to measure the difference between two localities, one being full of different pollutants (Sidi Salem) and the other being relatively clean (El Battah) and to evaluate the ability of D. trunculus to overcome the environmental stress during a transplantation experiment by a determination of fatty acid profile, the enzymes activities and the level of metallothioneins (MTs), a biomarker of metallic contamination. Adults of D. trunculus were collected at Sidi Salem (contaminated site) and transplanted into El Battah (reference site) for 21 days in cages (60 × 60 × 60 cm with a 2 mm mesh). Biochemical analyzes were conducted at different times (0, 7, 14 and 21 days). At 0-day experiment: the rate of the fatty acids, the enzymes activities and MT levels at the site of Sidi Salem (polluted site) were significantly different from those of El Battah. During the transplantation a gradual restoration of fatty acids rates, enzymes activities and MT levels was observed. At the end of the period of transplantation, the values are comparable to those of El Battah. A two-way ANOVA (time, site) on data revealed significant effects of time and site. Overally, D. trunculus is able to induce its detoxification system and to restore relatively rapidly the status of individuals from the reference site (El Battah).

Drill cuttings leave behind thousands of tons of residues without adequate treatment, generating a large environmental liability. Therefore knowledge about the microbial community of drilling residue may be useful for developing bioremediation strategies. In this work, samples of drilling residue were enriched in different culture media in the presence of petroleum, aiming to select potentially oil-degrading bacteria and biosurfactant producers. Total DNA was extracted directly from the drill cutting samples and from two enriched consortia and sequenced using the Ion Torrent platform. Taxonomic analysis revealed the predominance of Proteobacteria in the metagenome from the drill cuttings, while Firmicutes was enriched in consortia samples. Functional analysis using the Biosurfactants and Biodegradation Database (BioSurfDB) revealed a similar pattern among the three samples regarding hydrocarbon degradation and biosurfactants production pathways. However, some statistical differences were observed between samples. Namely, the pathways related to the degradation of fatty acids, chloroalkanes, and chloroalkanes were enriched in consortia samples. The degradation colorimetric assay using dichlorophenolindophenol as an indicator was positive for several hydrocarbon substrates. The consortia were also able to produce biosurfactants, with biosynthesis of iturin, lichnysin, and surfactin among the more abundant pathways. A microcosms assay followed by gas chromatography analysis showed the efficacy of the consortia in degrading alkanes, as we observed a reduction of around 66% and 30% for each consortium in total alkanes. These data suggest the potential use of these consortia in the bioremediation of drilling residue based on autochthonous bioaugmentation.