Amyl salicylate (AS) is a fragrance massively used as a personal care product and following the discharged in wastewaters may end up in the aquatic environment representing a potential threat for the ecosystem and living organisms. AS was recently detected in water of the Venice Lagoon, a vulnerable area continuously subjected to the income of anthropogenic chemicals. The lagoon is a relevant area for mollusc farming, including the Mediterranean mussels (Mytilus galloprovincialis) having an important economic and ecological role. Despite high levels of AS occurred in water of the Lagoon of Venice, no studies investigated the possible consequences of AS exposures on species inhabiting this ecosystem to date. For the first time, we applied a multidisciplinary approach to investigate the potential effects of the fragrance AS on Mediterranean mussels. To reach such a goal, bioaccumulation, cellular, biochemical, and molecular analyses (RNA-seq and microbiota characterization) were measured in mussels treated for 7 and 14 days with different AS Venice lagoon environmental levels (0.1 and 0.5 μg L⁻¹). Despite chemical investigations suggested low AS bioaccumulation capability, cellular and molecular analyses highlighted the disruption of several key cellular processes after the prolonged exposures to the high AS concentration. Among them, potential immunotoxicity and changes in transcriptional regulation of pathways involved in energy metabolism, stress response, apoptosis and cell death regulations have been observed. Conversely, exposure to the low AS concentration demonstrated weak transcriptional changes and transient increased representation of opportunistic pathogens, as Arcobacter genus and Vibrio aestuarianus. Summarizing, this study provides the first overview on the effects of AS on one of the most widely farmed mollusk species.

Fine particulate matter 2.5 (PM2.5) exposure leads to the progress of pulmonary disease. It has been reported that N6-methyladenosine (m6A) modification was involved in various biological processes and diseases. However, the critical role of m6A modification in pulmonary disease during PM2.5 exposure remains elusive. Here, we revealed that lung inflammation and mucus production caused by PM2.5 were associated with m6A modification. Both in vivo and in vitro assays demonstrated that PM2.5 exposure elevated the total level of m6A modification as well as the methyltransferase like 3 (METTL3) expression. Integration analysis of m6A RNA immunoprecipitation-seq (meRIP-seq) and RNA-seq discovered that METTL3 up-regulated the expression level and the m6A modification of Interleukin 24 (IL24). Importantly, we explored that the stability of IL24 mRNA was enhanced due to the increased m6A modification. Moreover, the data from qRT-PCR showed that PM2.5 also increased YTH N6-Methyladenosine RNA Binding Protein 1 (YTHDF1) expression, and the up-regulated YTHDF1 augmented IL24 mRNA translation efficiency. Down-regulation of Mettl3 reduced Il24 expression and ameliorated the pulmonary inflammation and mucus secretion in mice exposed to PM2.5. Taken together, our finding provided a comprehensive insight for revealing the significant role of m6A regulators in the lung injury via METTL3/YTHDF1-coupled epitranscriptomal regulation of IL24.

Bisphenol A (BPA) is widely used by manufacturers and in consumer products. Its release in the environment may affect male reproductive function. In this study, we examined the effect of low dose (0.1 mg/kg BW), short term exposure during puberty (PD21-35) on adult rat male reproduction. The results indicated that such exposure reset growth hormone (GH) and follicular stimulating hormone (FSH) homeostasis and resulted in a significantly higher level of serum testosterone without affecting serum luteinizing hormone level. QPCR and Western blot results showed that BPA significantly up-regulated selective genes/proteins in the Leydig cell steroidogenic pathway, including steroidogenic acute regulatory protein, cytochrome P450 11A1, cytochrome P450 17A, and low-density lipoprotein receptor. RNA-Seq analysis of testicular RNAs showed that BPA significantly affected the gene profiles of multiple testicular interstitial populations without affecting germ cells. Also, GO- and KEGG-analysis suggested that IGF1-related PI3K/AKT signaling was activated, which was confirmed by the increased phosphorylation of IRS1, AKT1 and CREB. The results indicated that a low-dose, short-term BPA exposure during puberty affected the adult male rat pituitary (GH and FSH) and testis (testosterone) homeostasis.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a well-known immunotoxic environmental pollutant. However, most immunotoxicology studies of TCDD were based on the animal models and the inner mechanisms have just focused on a few genes/proteins. In this study, the immune functions of THP-1-derived macrophages was measured with in-vitro bioassays after 24-h exposure of TCDD including environmentally relevant concentrations. RNA-seq and Weighted Gene Co-expression Network Analysis were used to characterize the immunotoxicity molecular mechanisms. Our study is the first report on the TCDD-induced effects of cell adhesion, morphology, and multiple cytokines/chemokines production on THP-1 macrophages. After TCDD treatment, we observed an inhibited cell adherence, probably attributed to the suppressed mRNA levels of adhesion molecules ICAM-1, VCAM-1 and CD11b, and a decrease in cell pseudopodia and expression of F-actin. The inflammatory cytokines TNF-α, IL-10 and other 8 cytokines/chemokines regulating granulocytes/T cells and angiogenesis were disrupted by TCDD. Alternative splicing event was found to be a sensitive target for TCDD. Using WGCNA, we identified 10 hub genes (TNF, SRC, FGF2, PTGS2, CDH2, GNG11, BDNF, WNT5A, CXCR5 and RUNX2) highly relevant to these observed phenotypes, suggesting AhR less important in the effects TCDD have on THP-1 macrophages than in other cells. Our findings broaden the understanding of TCDD immunotoxicity on macrophages and provide new potential targets for clarifying the molecular mechanisms.

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.

The Pearl River Estuary (PRE) is the largest estuary in southern China and under high metal stress. In the present study, we employed an integrated method of transcriptomics and proteomics to investigate the ecotoxicological effects of trace metals on the Hong Kong oyster Crassostrea hongkongensis. Three oyster populations with distinct spatial distributions of metals were sampled, including the Control (Station QA, the lowest metal levels), the High Cd (Station JZ, the highest Cd), and the High Zn–Cu–Cr–Ni (Station LFS, with the highest levels of zinc, copper, chromium, and nickel). Dominant metals in oysters were differentiated by principal component analysis (PCA), and theirgene and protein profiles were studied using RNA-seq and iTRAQ techniques. Of the 2250 proteins identified at both protein and RNA levels, 70 proteins exhibited differential expressions in response to metal stress in oysters from the two contaminated stations. There were 8 proteins altered at both stations, with the potential effects on mitochondria and endoplasmic reticulum by Ag. The genotoxicity, including impaired DNA replication and transcription, was specifically observed in the High Cd oysters with the dominating influence of Cd. The structural components (cytoskeleton and chromosome-associated proteins) were impaired by the over-accumulated Cu, Zn, Cr, and Ni at Station LFS. However, enhanced tRNA biogenesis and exosome activity might help the oysters to alleviate the toxicities resulting from their exposure to these metals. Our study provided comprehensive information on the molecular changes in oysters at both protein and RNA levels in responding to multi-levels of trace metal stress.

The wide range of industrial applications of chromium (Cr) has led to an increasing risk of water contamination by Cr(Ⅵ). However, efficient methods to remove or decrease the toxicity of Cr(Ⅵ) in situ are lacking. The main aim of this study was to investigate the mechanisms by which selenite alleviates chromium(Ⅵ)-induced toxicity in Chlamydomonas reinhardtii. Our results showed that K₂Cr₂O₇ had toxic effects on both the structure and physiology of C. reinhardtii in a dose-dependent manner. Adding selenite significantly alleviated chromium accumulation and toxicity in cells. RNA-seq data showed that the expression level of selenoproteins such as SELENOH was significantly increased. Both SELENOH-amiRNA knockdown mutants and selenoh insertional mutant produced more reactive oxygen species (ROS) and grew slower than the wild type, suggesting that SELENOH can reduce chromium toxicity by decreasing the levels of ROS produced by Cr(Ⅵ). We also demonstrated that selenite can reduce the absorption of Cr(Ⅵ) by cells but does not affect the process of Cr(Ⅵ) adsorption and efflux. This information on the molecular mechanism by which selenite alleviates Cr(Ⅵ) toxicity can be used to increase the bioremediation capacity of algae and reduce the human health risks associated with Cr(Ⅵ) toxicity.

Nitrate is a major pollutant component in ambient PM₂.₅. It is known that chronic exposure to PM₂.₅ NO₃⁻ damages respiratory functions. We aim to explore the underlying toxicological mechanism at single cell resolution.We systematically conducted exposure experiments on forty C57BL/6 mice, assessed respiratory functions, and profiled lung transcriptome. . Afterward, we estimated the cell type compositions from RNA-seq data using deconvolution analysis. The genes and pathways associated with respiratory function and dysregulated by to PM₂.₅ NO₃⁻ exposure were characterized at bulk-tissue and single-cell resolution.PM₂.₅ NO₃⁻ exposure did not significantly modify the cell type composition in lung, but profoundly altered the gene expression within each cell type. At ambient concentration (22 μg/m³), exposure significantly (FDR<10%) altered 95 genes’ expression. Among the genes associated with respiratory functions, a large fraction (74.6–91.7%) were significantly perturbed by PM₂.₅ NO₃⁻ exposure. For example, among the 764 genes associated with peak expiratory flow (PEF), 608 (79.6%) were affected by exposure (p = 1.92e-345). Pathways known to play role in lung disease pathogenesis, including circadian rhythms, sphingolipid metabolism, immune response and lysosome, were found significantly associated with respiratory functions and disrupted by PM₂.₅ NO₃⁻ exposure.This study extended our knowledge of PM₂.₅ NO₃⁻ exposure’s effect to the levels of lung gene expression, pathways, lung cell type composition and cell specific transcriptome. At single cell resolution, we provided insights in toxicological mechanism of PM₂.₅ NO₃⁻ exposure and subsequent pulmonary disease risks.

In this study, an arsenic (As)-resistant facultative endophytic bacterial strain, F2, was isolated from the root of Oryza sativa Longliangyou Huazhan and identified as Serratia liquefaciens according to 16S rRNA gene sequence analysis. Strain F2 was characterized for i) its impacts on As immobilization in solution and rice tissue As accumulation, and ii) the mechanisms involved for different levels of As-pollution in soils. In strain F2-inoculated culture medium, the concentration of As decreased, while the pH, cell growth, and cell-immobilized As significantly increased over time. Grain As content reduced by between 23 and 36% in strain F2-inoculated rice plants in comparison to the control. Available As content decreased by between 28 and 52%, but unavailable As content increased by between 27 and 46% in the strain F2-inoculated soil when compared with the controls. Moreover, the strain decreased the As translocation factor by between 34 and 46%, but increased the As concentration by between 24 and 70% in Fe plaque on the rice root surfaces in comparison to the controls. These results suggested that strain F2 decreased the rice grain As uptake by i) decreasing available As in soil, ii) increasing rice root surface As adsorption, and iii) decreasing As translocation from the roots to grains. Our findings may provide a new rice-derived facultative endophytic bacteria-assisted approach for decreasing the As uptake to rice grains in As-polluted soils.

Wastewater containing high concentrations of nitriles, if discharged without an appropriate nonhazardous disposal strategy, will cause serious environmental pollution. During secondary sewage biological treatment, most existing bacteria cannot endure high-concentration nitriles due to poor tolerance and low degradation ability. The Rhodococcus rhodochrous strain BX2 screened by our laboratory shows high resistance to nitriles and can efficiently degrade these compounds. Compared with sole high-concentration nitriles present in the biodegradation process, the addition of glucose at a suitable concentration can effectively increase the biomass of BX2, promote the expression of nitrile-degrading enzyme genes, improve the activities of these enzymes and enhance the pollutant removal efficiency via carbon catabolite repression (CCR) mechanisms. Whole-genome sequencing revealed that the four key regulators of CCR identified in gram-negative and gram-positive bacteria are concomitant in BX2. This study provides an economically feasible strategy for the microbial remediation of high-concentration nitriles and other organic pollutants.