Fluoride is a well-known compound for its usefulness in healing dental caries. Similarly, fluoride is also known for its toxicity to various tissues in animals and humans. It causes skeletal fluorosis leading to osteoporosis of the bones. We hypothesized that when bones are affected by fluoride, the skeletal muscles are also likely to be affected by underlying molecular events involving myogenic differentiation. Murine myoblasts C2C12 were cultured in differentiation media with or without NaF (1 ppm-5 ppm) for four days. The effects of NaF on myoblasts and myotubes when exposed to low (1.5 ppm) and high concentration (5 ppm) were assessed based on the proliferation, alteration in gene expression, ROS production, and production of inflammatory cytokines. Changes based on morphology, multinucleated myotube formation, expression of MyHC1 and signaling pathways were also investigated. Concentrations of NaF tested had no effects on cell viability. NaF at low concentration (1.5 ppm) caused myoblast proliferation and when subjected to myogenic differentiation it induced hypertrophy of the myotubes by activating the IGF-1/AKT pathway. NaF at higher concentration (5 ppm), significantly inhibited myotube formation, increased skeletal muscle catabolism, generated reactive oxygen species (ROS) and inflammatory cytokines (TNF-α and IL-6) in C2C12 cells. NaF also enhanced the production of muscle atrophy-related genes, myostatin, and atrogin-1. The data suggest that NaF at low concentration can be used as muscle enhancing factor (hypertrophy), and at higher concentration, it accelerates skeletal muscle atrophy by activating the ubiquitin-proteosome pathway.

To trace the circulation history of aquatic bioavailable Hg in the Antarctic, the species and isotopic compositions of Hg in sediment, Archaeogastropoda (Agas), Neogastropoda (Ngas), and fish collected from King George Island were studied in detail. Positive mass independent fractionation (MIF) was observed and positively correlated with the percentages of methylmercury (MeHg%) in Agas and Ngas, suggesting an effect of MeHg accumulation during trophic transfer on MIF signatures. However, both the ratios of Δ199Hg/δ202Hg and Δ199Hg/Δ201Hg indicated different circulation histories of Hg in Agas, Ngas, and fish. The microbial methylation in sediment was the primary source of MeHg in Agas and Ngas (Δ199Hg/δ202Hg ∼0, Δ199Hg/Δ201Hg ∼1.00). In contrast, the MeHg in fish (Δ199Hg/δ202Hg = 0.55 ± 0.06, Δ199Hg/Δ201Hg = 1.19 ± 0.17) came from the combined sources of residual MeHg which had sunk from the surface water and microbial-methylated MeHg in sediments, and the bioavailable Hg in the sediments contributed to approximately 44% of the total Hg in fish. Subsequently, the Δ199Hg values of bioavailable MeHg and IHg in sediments were quantitatively calculated, which provided key end-member information for future source apportionment in the Antarctic and other pelagic regions. It was also found that the Hg accumulated in Agas and Ngas had no history of MeHg photo-degradation, indicating that the methylated Hg in benthic zones suffered little photo-degradation and thus presented high bioavailability and environmental risk.

Swine waste is a reservoir of microbial pollutants, including pathogens, antibiotic resistance genes (ARGs) and antibiotic resistant bacteria (ARB); therefore, soil fertilized with swine waste is an essential pathway for the dissemination of microbial pollutants from concentrated swine farms to the public. To rationalize the intervals of swine wastes application and investigate the effects of soil type on the occurrences of microbial pollutants and antibiotic resistance, pot experiments were conducted with three typical soils, humic acrisol, calcaric cambisols and histosols, being collected from south, northwest and northeast China (soil-R, soil-Y and soil-B, respectively). The soils were amended with swine slurry, digestate and chemical fertilizers and then conducted for 172 days. The influence of microbial pollutants and antibiotic resistance in soil posed by digestate application was similar to that of the chemical fertilizers, while swine slurry posed high risks to the soil. Soil-B which had the highest organic matter and neutral pH was least influenced by the swine slurry amendment. tetG, tetM and ermF were persistent ARGs in the slurry treated soil, and their decay rates fitted to first-order kinetics in the order soil-B> soil-Y > soil-R. Putative pathogens showed strong correlations with ARGs, suggesting a risk of dissemination. The initial 43–82 days was the active phase of microbial pollution in slurry treated soil, during which time heavy metals, moisture content, total organic carbon and the microbial community were key factors contributing to changes in antibiotic resistance. Fertilization intervals of livestock wastes should be lengthened over the ARG active phase.

Groundwater in the Chalk aquifer is an important water resource whose quality has degraded due to fertilizer and pesticide use. Atrazine, classified as a priority substance, has been one of the most applied pesticides and also one of the most frequently detected pesticides in groundwater. The present study investigated the transfer and degradation of atrazine in the unsaturated zone of the Chalk aquifer in Northern France. The study was conducted in an underground quarry (Saint-Martin-le-Noeud), which provides a direct access to the water table and intercepts the unsaturated zone at different depths. The lake and the ceiling percolation of 16 sites throughout the quarry were followed. For 16 sites, the percolating flow rate and lake level were measured and the lake water was sampled for nitrate, atrazine and deethylatrazine (DEA, main degradation product of atrazine) analysis over 2.5 years. High spatial variations in hydrodynamics (percolating flow rate and lake level) and in lake water quality (atrazine between 55±11 and 202±40 ng L−1 and DEA between 269±53 and 1727±345 ng L−1) indicate that the properties of the unsaturated zone influence the transfer and the degradation of atrazine. A counterclockwise hysteresis characterizes the relationship between the lake level and atrazine concentration. Temporal variation shows that the atrazine is transferred through the matrix and fractures with a delay caused by the sorption process that differs in atrazine and DEA. The layer of clay-with-flints is shown to favor the degradation of atrazine near the surface. Preferential pathways may be created below clay-with-flints, through which the transfer of atrazine is quicker.

The oriental river prawn, Macrobrachium nipponense, is an important breeding species in China. The ovary development of this prawn is regulated by the genetic factors and external environmental factors and has obvious seasonal regularity. However, the molecular mechanism of regulating ovary degradation in M. nipponense remains unclear. To address this issue, we performed transcriptome sequencing and gene expression analyses of eyestalks, cerebral ganglia (CG) and thoracic ganglia (TG) of female M. nipponense between the full ovary stage and degenerate ovary stage. Differentially expressed genes enrichment analysis results identified several important pathways such as “phototransduction-fly,” “circadian rhythm-fly” and “steroid hormone biosynthesis secretion.” In the period of ovarian degeneration, the expressions of Tim, Per2 and red pigment concentration hormone (RPCH) were significantly decreased in the eyestalk, CG and TG. And expression of 7 genes in the steroid synthesis pathway, including steryl-sulfatase, cytochrome P450 family 1 subfamily A polypeptide 1, estradiol 17β-dehydrogenase 2, glucuronosyltransferase, 3-oxo-5-alpha-steroid 4-dehydrogenase 1, estradiol 17-dehydrogenase 1 and estrone sulfotransferase was significantly decreased in the CG. Food and light signals affect the expression of clock genes and thereby decrease the expression of RPCH and the estradiol synthesis-related genes in the nervous system, which may be the main cause of ovarian degeneration in M. nipponense. The results will contribute to a better understanding of the molecular mechanisms of ovarian development regulation in crustaceans.

High resolution sediment records in the Yangtze Delta front were constructed to reveal recent environmental changes in response to river basin human activities. Increases in nutrient and organic C influxes that began in the 1950s, together with elevated primary productivity and increased chemical fertilizer application, suggested a shift toward anthropogenic-predominated environmental changes during this period. The depletion of total organic C (TOC), total N (TN), and biogenic Si (BSi), along with the decline in sedimentation rate and coarsening of sediment coincided with the development of hydrological engineering in the river basin from the 1980s. Reservoir Si retention substantially altered river mouth primary productivity community composition from diatoms to non-diatoms, thereby changing the BSi/TOC molar ratio in the sediment profile. Estimation of biogenic component burial fluxes was conducted to assess the variation and potential impacts. A recent dramatic decline in biogenic component burial in the delta area suggested a low nutrient removal efficiency in this region, due to the decrease in sediment discharge. Consequently, more nutrients have been further transported to the inner shelf and open waters instead of being buried in the delta sediment, thereby increasing the environmental pressure in the Yangtze Delta and adjoining coastal area.

One attraction of using hydrochar (HC) and biochar (BC) in soil is their intrinsic affinity for organic contaminants. Oxidative ageing is likely to induce changes in physicochemical properties and functionality. To explore the long-term potential trajectories for corn stalk HC and BC to adsorb organic pollutants, we employed HC and BC exposure in 5% H2O2 to simulate oxidative ageing and get insights into mechanisms of atrazine adsorption on fresh and artificially aged materials. The physicochemical properties of fresh and aged materials were systematically compared using elemental analysis, SSA, FTIR, XPS and SEM-EDS, alongside K2Cr2O7/H2SO4 treatment to assess chemical oxidation stability. Atrazine is a typical herbicide chemical and hydrophobic organic pollutant. Adsorption isotherms of atrazine were used to reveal differences in mechanisms of sorption to BC and HC, by assessment before and ageing. BC freshly produced at 650 °C displayed higher capacity for atrazine sorption than BC produced at 500 °C, with a dominant role for π-π EDA interactions. The sorption capacity of HC freshly produced at 250 °C was higher than for HC produced at 200 °C HC, owing to higher C content and atrazine partitioning into the organic phase. Ageing increased the surface abundance of oxygenated functional groups for BC and HC and diminished bulk aromaticity. After ageing, atrazine sorption by high temperature BC was lower, but for HC it was increased. Such divergent effects must be considered when developing strategies to co-manage contaminants and carbon through the addition of carbonized materials to land.

Deoxynivalenol (DON) frequently detected in a wide range of foods and feeds, inducing cytotoxicity to animals and humans. To investigate the underlying mechanism of DON-induced apoptosis and inflammation in porcine small intestinal epithelium, intestinal porcine epithelial cells (IPEC-J2 cells) were chosen as objects, and were treated by different concentrations (0 μg/mL, 0.2 μg/mL, 0.5 μg/mL, 1.0 μg/mL, 2.0 μg/mL, 4.0 μg/mL, 6.0 μg/mL) of DON. The results showed that DON induced cytotoxicity of IPEC-J2 cells in a dose-dependent manner, which is demonstrated by decreasing cell viability. Compared with the control group, DON treatment increased the expressions of genes associated with inflammation and apoptosis, such as interleukin-1 beta (IL-1β), cyclooxgenase-2 (COX-2), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), caspase-3, caspase-8, caspase-9, and decreased the cell anti-oxidative status. Protein immunofluorescence showed increased expression of caspase-3, nuclear factor kB (NF-κB) and phosphorylated NF-κB in IPEC-J2 cells. DON increased the content of intracellular reactive oxygen species (ROS) of IPEC-J2 cells. N-Acetyl-L-cysteine (NAC), a commonly used antioxidant, blocked DON-induced ROS generation, alleviated the DON-induced apoptosis and inflammation. These results suggested that DON-induced impairment of IPEC-J2 cells is possibly due to increased ROS production, and expressions of genes and proteins associated with apoptosis and inflammation.

Fine dust (FD) is a form of air pollution and is responsible for a wide range of diseases. Specially, FD is associated with several cardiovascular diseases (CVDs); long-term exposure to FD was shown to decrease endothelial function, but the underlying mechanism remains unclear. We investigated whether exposure to FD causes premature senescence-associated endothelial dysfunction in endothelial cells (ECs) isolated from porcine coronary arteries. The cells were treated with different concentrations of FD and senescence associated-beta galactosidase (SA-β-gal) activity, cell cycle progression, expression of endothelial nitric oxide synthase (eNOS), oxidative stress level, and vascular function were evaluated. We found that FD increased SA-β-gal activity, caused cell cycle arrest, and increased oxidative stress, suggesting the premature induction of senescence; on the other hand, eNOS expression was downregulated and platelet aggregation was enhanced. FD exposure impaired vasorelaxation in response to bradykinin and activated the local angiotensin system (LAS), which was inhibited by treatment with the antioxidant N-acetyl cysteine (NAC) and angiotensin II receptor type 1 (AT₁) antagonist losartan (LOS). NAC and LOS also suppressed FD-induced SA-β-gal activity, increased EC proliferation and eNOS expression, and improved endothelial function. These results demonstrate that FD induces premature senescence of ECs and is associated with increased oxidative stress and activation of LAS. This study can serve as a pharmacological target for prevention and/or treatment of air pollution-associated CVD.