The mechanisms underlying cobalt toxicity in aquatic species in general and cnidarians in particular remain poorly understood. Herein we investigated cobalt toxicity in a Hydra model from morphological, histological, developmental, and molecular biological perspectives. Hydra, exposed to cobalt (0–60 mg/L), were altered in morphology, histology, and regeneration. Exposure to standardized sublethal doses of cobalt impaired feeding by affecting nematocytes, which in turn affected reproduction. At the cellular level, excessive ROS generation, as the principal mechanism of action, primarily occurred in the lysosomes, which was accompanied by the upregulation of expression of the antioxidant genes SOD, GST, GPx, and G6PD. The number of Hsp70 and FoxO transcripts also increased. Interestingly, the upregulations were higher in the 24-h than in the 48-h time-point group, indicating that ROS overwhelmed the cellular defense mechanisms at the latter time-point. Comet assay revealed DNA damage. Cell cycle analysis indicated the induction of apoptosis accompanied or not by cell cycle arrest. Immunoblot analyses revealed that cobalt treatment triggered mitochondria-mediated apoptosis as inferred from the modulation of the key proteins Bax, Bcl-2, and caspase-3. From this data, we suggest the use of Hydra as a model organism for the risk assessment of heavy metal pollution in aquatic ecosystems.

Perfluorooctanoic acid (PFOA) has received an increasing attention in the agricultural and food industries due to its risk to human health. To facilitate the development of novel biomarkers of Escherichia coli against PFOA through multi-omics technologies, and to reveal the resistance mechanism of E. coli against PFOA at protein levels, the interactions among pollutant stress, protein expression and cell metabolism was investigated by using iTRAQ-based quantitative proteomic analysis. The results revealed that the 63 up-regulated proteins mainly involved in tricarboxylic acid cycle, glyoxylate and dicarboxylate metabolism and fatty acid biosynthesis, whereas, the 69 down-regulated proteins related to oxidative phosphorylation, pyruvate metabolism and the cell cycle-caulobacter pathway, were also associated with the increase of membrane permeability, excessive expenditure of ATP, disruption of fatty acid biosynthesis under PFOA stress. The results provide novel insights into the influence mechanisms of PFOA on fatty acid and protein networks.

Uptake and accumulation by plants is a significant pathway in the migration and transformation of phthalate esters (PAEs) in the environment. However, limited information is available on the mechanisms of PAE metabolism in plants. Here, we investigated the metabolism of di-n-butyl phthalate (DnBP), one of the most frequently detected PAEs, in pumpkin (Cucurbita moschata) seedlings via a series of hydroponic experiments with an initial concentration of 10 mg L⁻¹. DnBP hydrolysis occurred primarily in the root, and two of its metabolites, mono-n-butyl phthalate (MnBP) and phthalic acid (PA), were detected in all plant tissues. The MnBP concentration was an order of magnitude higher than that of PA in shoots, which indicated MnBP was more readily transported to the shoot than was PA because of the former's dual hydrophilic and lipophilic characteristics. More than 80% of MnBP and PA were located in the cell water-soluble component except that 96% of MnBP was distributed into the two solid cellular fractions (i.e., cell wall and organelles) at 96 h. A 13–20% and 29–54% increase of carboxylesterase (CXE) activity shown in time-dependent and concentration-dependent experiments, respectively, indicated the involvement of CXEs in plant metabolism of DnBP. The level of CXE activity in root subcellular fractions was in the order: the cell water-soluble component (88–94%) >> cell wall (3–7%) > cell organelles (3–4%), suggesting that the cell water-soluble component is the dominant locus of CXE activity and also the domain of CXE-catalyzed hydrolysis of DnBP. The addition of triphenyl phosphate, a CXE inhibitor, led to 43–56% inhibition of CXE activity and 16–25% increase of DnBP content, which demonstrated the involvement of CXEs in plant metabolism of DnBP. This study contributes to our understanding of enzymitic mechanisms of PAE transformation in plants.

The area of agriculturally used land and following to that the use of pesticides are steadily increasing. Insecticides do not only reduce pest organisms on crops but can also affect non-target organisms when present in sublethal concentrations in the environment. We investigated the effects of an exposure to sublethal pyrethroid (lambda-cyhalothrin) concentrations, at doses 20 and 60 times lower than the LC50, respectively, on reproductive traits and adult cuticular hydrocarbon (CHC) profiles of a leaf beetle (Phaedon cochleariae Fabricius). Furthermore, we tested for effects on growth and antennae symmetry of the offspring generation that was not exposed to the insecticide. Sublethal insecticide concentrations decreased the egg number produced by the adults and the hatching rate. Moreover, the chemical phenotype (CHC profile) of adults was altered in dependence of the insecticide treatment, with sex-specific effects. In the unexposed offspring of insecticide-exposed parents, a prolonged development time and a fluctuating asymmetry of the females' antennae were detected, revealing transgenerational effects. The insecticide effects on the CHC profiles of the parental generation might have been caused by changes in CHC precursors, which were potentially induced by the insecticide treatment of the insect diet. Such altered CHC pattern may have implications for intraspecific communication, e.g., in mate choice, as well as in an interspecific way, e.g., in interactions with other arthropod species. The observed detrimental transgenerational effects might be explainable by a reduced investment in the offspring, maternal transfer or epigenetic processes. An asymmetry of the antennae may lead to defects in the reception of chemical signals. In conclusion, the results disclose that, besides detrimental (transgenerational) effects on reproduction and development, an exposure to sublethal insecticide concentrations can impair the chemical communication between individuals, with impacts on the sender (i.e., the CHC profile) and the receiver (i.e., caused by asymmetry of the antennae).

Polybrominated diphenyl ethers (PBDEs) have been used in a broad array of polymeric materials such as plastics, foams, resins and adhesives to inhibit the spread of fires since the 1970s. The widespread environmental contamination and well documented toxic effects of PBDEs have led to bans and voluntary withdrawals in many jurisdictions. Replacement novel brominated flame retardants (NBFRs) have, however, exhibited many of the same toxic characteristics as PBDEs and appear to share similar environmental fate. This paper presents a critical review of the scientific literature regarding PBDE and NBFR contamination of surface soils internationally, with the secondary objective of identifying probable pollution sources. An evaluation of NBFR distribution in soil was also conducted to assess the suitability of the newer compounds as replacements for PBDEs, with respect to their land contamination potential. Principle production of PBDEs and NBFRs and their consequent use in secondary polymer manufacture appear to be processes with strong potential to contaminate surrounding soils. Evidence suggests that PBDEs and NBFRs are also released from flame retarded products during disposal via landfill, dumping, incineration and recycling. While the land application of sewage sludge represents another major pathway of soil contamination it is not considered in this review as it is extensively covered elsewhere. Both PBDEs and NBFRs were commonly detected at background locations including Antarctica and northern polar regions. PBDE congener profiles in soil were broadly representative of the major constituents in Penta-, Octa- and Deca-BDE commercial mixtures and related to predicted market place demand. BDE-209 dominated soil profiles, followed by BDE-99 and BDE-47. Although further research is required to gain baseline data on NBFRs in soil, the current state of scientific literature suggests that NBFRs pose a similar risk to land contamination as PBDEs.

Based on the breast cancer cells and the vascular endothelial cells are both estrogen-sensitive, we proposed a close reciprocity existed between them in the tumor microenvironment, via shared molecular mechanism affected by environmental endocrine disruptors (EDCs). In this study, bisphenol A (BPA), via triggering G-protein estrogen receptor (GPER), stimulated cell proliferation and migration of bovine vascular endothelial cells (BVECs) and breast cancer cells (SkBr-3 and MDA-MB-231) and enhanced tumor growth in vivo. Moreover, the expression of both hypoxia inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) were up-regulated in a GPER-dependent manner by BPA treatment under hypoxic condition, and the activated GPER induced the HIF-1α expression by competitively binding to caveolin-1 (Cav-1) and facilitating the release of heat shock protein 90 (HSP90). These findings show that in a hypoxic microenvironment, BPA promotes HIF-1α and VEGF expressions through a shared GPER/Cav-1/HSP90 signaling cascade. Our observations provide a probable hypothesis that the effects of BPA on tumor development are copromoting relevant biological responses in both vascular endothelial and breast cancer cells.

To examine the effects of BaP on tissue apoptosis, laboratory studies were conducted using juvenile Chinese rare minnows (Gobiocypris rarus) exposed to 1, 5, 20, and 80 μg/L of BaP for 28 days. The post-treatment pathological findings in the liver were associated with hepatocyte swelling, karyopyknosis, and karyorrhexis. Moreover, an increase in the goblet cells in the intestine, epithelial hyperplasia of the gills and fusion of gill lamellae were observed. Significant increases in hepatocyte apoptosis using the TUNEL stain were observed in the liver tissue but not in the intestine and gills. In addition, BaP exposure significantly up-regulated the mRNA levels of cyp1a1, p53, bax, bcl-2, and caspase-9 in the liver following the 5, 20, and 80 μg/L treatments, whereas the apaf-1 was significantly down-regulated following all treatments. Moreover, the activities of caspase 3 and caspase 8 were markedly elevated, whereas the protein expression levels of Apaf-1 were down-regulated following the 20 and 80 μg/L treatments. Taken together, our results suggested that BaP strongly induces tissue-specific apoptosis in vivo, leading to significant pathological changes. The responsiveness of apoptotic-related genes demonstrates that BaP induced apoptosis in the liver may be through a mitochondria-independent pathway.

Transport of coal by train through residential neighborhoods in Metro Vancouver, British Columbia, Canada may increase the possibility of exposure to particulate matter at different size ranges, with concomitant potential negative health impacts. This pilot study identifies and quantifies train impacts on particulate matter (PM) concentrations at a single location. Field work was conducted during August and September 2014, with the attributes of a subset of passing trains confirmed visually, and the majority of passages identified with audio data. In addition to fixed ground based monitors at distances 15 and 50 m from the train tracks, an horizontally pointing mini-micropulse lidar system was deployed on three days to make backscatter and depolarization measurements in an attempt to identify the zone of influence, and sources, of train-generated PM. Ancillary wind and dust fall data were also utilized. Trains carrying coal are associated with a 5.3 (54%), 4.1 (33%), and 2.6 (17%) μgm−3 average increase in concentration over a 14 min period compared to the average concentrations over the 10 min prior to and after a train passage (“control” or “background” conditions), for PM3, PM10, and PM20, respectively. In addition, for PM10 and PM20, concentrations during train passages of non-coal-carrying trains were not found to be significantly different from PM concentrations during control conditions. Presence of coal dust particles at the site was confirmed by dust fall measurements. Although enhancements of PM concentrations during 14 min train passages were generally modest, passing coal trains occasionally enhanced concentrations at 50 m from the tracks by ∼100 μgm-3. Results showed that not every train passage increased PM concentrations, and the effect appears to be highly dependent on wind direction, local meteorology and load related factors. LiDAR imagery suggests that re-mobilization of track-side PM by train-induced turbulence may be a significant contributor to coarse particle enhancements.

The increased use of pesticides has caused concern over the possible direct association of exposure to combinations of these compounds with bee health problems. There is growing proof that bees are regularly exposed to mixtures of agrochemicals, but most research has been focused on managed bees living in farmland, whereas little is known about exposure of wild bees, both in farmland and urban habitats. To determine exposure of wild bumblebees to pesticides in agricultural and urban environments through the season, specimens of five different species were collected from farms and ornamental urban gardens in three sampling periods. Five neonicotinoid insecticides, thirteen fungicides and a pesticide synergist were analysed in each of the specimens collected. In total, 61% of the 150 individuals tested had detectable levels of at least one of the compounds, with boscalid being the most frequently detected (35%), followed by tebuconazole (27%), spiroxamine (19%), carbendazim (11%), epoxiconazole (8%), imidacloprid (7%), metconazole (7%) and thiamethoxam (6%). Quantifiable concentrations ranged from 0.17 to 54.4 ng/g (bee body weight) for individual pesticides. From all the bees where pesticides were detected, the majority (71%) had more than one compound, with a maximum of seven pesticides detected in one specimen. Concentrations and detection frequencies were higher in bees collected from farmland compared to urban sites, and pesticide concentrations decreased through the season. Overall, our results show that wild bumblebees are exposed to multiple pesticides when foraging in agricultural and urban landscapes. Such mixtures are detected in bee tissues not just during the crop flowering period, but also later in the season. Therefore, contact with these combinations of active compounds might be more prolonged in time and widespread in the environment than previously assumed. These findings may help to direct future research and pesticide regulation strategies to promote the conservation of wild bee populations.

In this study, we systematically investigated the effect of multiwall carbon nanotubes (MWCNTs) on the removal of tetrabromobisphenol A (TBBPA) mediated by horseradish peroxidase (HRP) at varying important conditions. The results suggested that the presence of MWCNTs significantly enhanced the removal of TBBPA mediated by HRP and the reaction rate constant was linear with the MWCNTs dosage. The enhancement of MWCNTs on the HRP-mediated reaction was attributed to two facts, one is that MWCNTs protected HRP from inactivation, the other is that the presence of MWCNTs made the homogeneous reaction of TBBPA be heterogeneous reaction by adsorbing TBBPA on its surface. Moreover, the influence of MWCNTs on TBBPA products distribution was further elucidated. We found that the species of reaction product had no difference between the HRP-mediated systems with and without the presence of MWCNTs. However, the presence of MWCNTs significantly decreased the yields of each product. These results give insight into the role of MWCNTs in HRP-mediated TBBPA reactions and provide theoretical foundation for potential development of novel enzymatic methods to control TBBPA contamination.MWCNTs enhanced the removal of TBBPA mediated by HRP/H2O2, because it protected HRP from inactivation and adsorbed TBBPA on its surface to form a heterogeneous reaction process.