Ground-level ozone (O3) concentrations have been elevating in the last century. While there has been a notable progress in understanding O3 effects on vegetation, O3 effects on ecological stoichiometry remain unclear, especially early in the oxidative stress. Ethyelenediurea (EDU) is a chemical compound widely applied in research projects as protectant of plants against O3 injury, however its mode of action remains unclear. To investigate O3 and EDU effects early in the stress, we sprayed willow (Salix sachalinensis) plants with 0, 200 or 400 mg EDU L−1, and exposed them to either low ambient O3 (AOZ) or elevated O3 (EOZ) levels during the daytime, for about one month, in a free air O3 controlled exposure (FACE); EDU treatment was repeated every nine days. We collected samples for analyses from basal, top, and shed leaves, before leaves develop visible O3 symptoms. We found that O3 altered the ecological stoichiometry, including impacts in nutrient resorption efficiency, early in the stress. The relation between P content and Fe content seemed to have a critical role in maintaining homeostasis in an effort to prevent O3-induced damage. Photosynthetic pigments and P content appeared to play an important role in EDU mode of action. This study provides novel insights on the stress biology which are of ecological and toxicological importance.

Microcystin-LR (MC-LR) is the most abundant toxicant among microcystin variants produced by cyanobacteria. MC-induced toxicity is broadly reported to pose a threat to aquatic animals and humans and has been associated with the dysfunction of some organs such as liver and kidney. However, MC-induced neurotoxicity has not been well characterized after long-term exposure. This study was designed to investigate the neurotoxic effects after chronic oral administration of MC-LR. In our trial, C57/BL6 mice received MC-LR at 0, 1, 5, 10, 20 and 40 μg/L in drinking water for twelve months. Our data demonstrated that mitochondrial DNA (mtDNA) damage was evident in the damaged neurons as a result of chronic exposure. Histopathological abnormalities and mtDNA damage were observed in the hippocampus and cerebral cortex. Furthermore, MC-LR exerted distinct effects on these two brain regions. The hippocampus was more susceptible to the treatment of MC-LR compared with the cerebral cortex. However, no strong relationships were observed between the genotoxic effects and exposure doses. In conclusion, this study has provided a mtDNA-related mechanism for underlying chronic neurotoxicity of MC-LR and suggested the presence of differential toxicant effects on the hippocampus and cerebral cortex.

Plants have the ability to adapt themselves under stressed conditions through reprogramming their growth and development. Understanding the mechanisms regulating overall growth of stressed plant is an important issue for plant and environmental biology research. Although the role of NO in modulating arsenic (As) toxicity is known, nitric oxide (NO) induced alteration in auxin and nutrient related transporters during As stress in rice is poorly understood. Experimental results showed that As exposure decreased gene expression level of polar auxin transporter (PIN proteins), and nutrient transporter related genes (AMT, NRT, NiR, PHT, KTP). The improved tolerance induced by As + NO combination is attributed to reduced As accumulation in rice seedlings, improved root architectural changes, overall growth of plant, chlorophyll, protein content, and accumulation of mineral nutrients by reducing the ROS generation. Further, enhanced transcript levels of PIN proteins and mineral nutrition related genes were also observed under As + NO treatment. Additional biochemical data revealed enhanced oxidative stress by increasing the level of antioxidant enzymes, and stress-related parameters. Overall, the study provides an integrated view of plant response during As + NO interaction to change the plant metabolism through different cellular processes.

Microplastics may lose buoyancy and occur in deeper waters and ultimately sink to the sediment and this may threaten plankton inhabiting in various water layers and benthic organisms. Here, we conduct the first survey on microplastics in the water column and corresponding sediment in addition to the surface water in the Bohai Sea. A total of 20 stations covering whole Bohai Sea were selected, which included 6 stations specified for water column studying. Seawater was sampled every 5 m, with maximal depth of 30 m in the water column using Niskin bottles coupled with a ship-based conductivity, temperature and depth sensor (CTD) system and surface sediment samples were collected using box corer. The results indicated that higher microplastic levels accumulated at a depth range of 5–15 m in the water column in some stations, suggesting the surface water survey was not sufficient to reflect microplastics loading in a water body. Fibers predominated microplastic types in both seawater and sediment of the Bohai Sea, which accounted for 75%–96.4% of the total microplastics. However the relatively proportion of the fibers in the deeper water layers and sediment was lower than that in the surface water. Microplastic shapes are more diverse in the sediment than in the seawater in general. The microplastic sizes changed with depth in the water column and the proportion of the size-fraction < 300 μm increased with depth, probably as a result of rapid biofouling on the small microplastics due to their higher specific surface area. Such depth distribution also implied that sampling with manta net (>330 μm) that commonly used in the oceanographic survey might underestimate microplastics abundance in the water column. Further studies are recommended to focus on the sinking behavior of microplastics and their effects on marine organisms.

Dietary consumption of contaminated vegetables may contribute to polycyclic aromatic hydrocarbon (PAH) exposure in humans; however, this exposure pathway has not been examined thoroughly. This study aims to characterize the concentrations of PAHs in six types of vegetables grown near industrial facilities in Shanghai, China. We analyzed 16 individual PAHs on the US EPA priority list, and the total concentration in vegetables ranged from 65.7 to 458.0 ng g−1 in the following order: leafy vegetables (romaine lettuce, Chinese cabbage and Shanghai green cabbage) > stem vegetables (lettuce) > seed and pod vegetables (broad bean) > rhizome vegetables (daikon). Vegetable species, wind direction, and local anthropogenic emissions were determinants of PAH concentrations in the edible part of the vegetable. Using isomer ratios and principal component analysis, PAHs in the vegetables were determined to be mainly from coal and wood combustion. The sources of PAHs in the six types of vegetables varied. Daily ingestion of PAHs due to dietary consumption of these vegetables ranged from 0.71 to 14.06 ng d−1 kg−1, with contributions from Chinese cabbage > broad bean > romaine > Shanghai green cabbage > lettuce > daikon. The daily intake doses adjusted by body weight in children were higher than those in teenagers and adults. Moreover, in adults, higher concentrations of PAHs were found in females than in males. For individuals of different age and gender, the incremental lifetime cancer risks (ILCRs) from consuming these six vegetables ranged from 4.47 × 10−7 to 6.39 × 10−5. Most were higher than the acceptable risk level of 1 × 10−6. Our findings demonstrate that planting vegetables near industrial facilities may pose potential cancer risks to those who consume the vegetables.

Recent studies have indicated that urban streets can be hotspots for emissions of methane (CH4) from leaky natural gas lines, particularly in cities with older natural gas distribution systems. The objective of the current study was to determine whether leaking sewer pipes could also be a source of street-level CH4 as well as nitrous oxide (N2O) in Cincinnati, Ohio, a city with a relatively new gas pipeline network. To do this, we measured the carbon (δ13C) and hydrogen (δ2H) stable isotopic composition of CH4 to distinguish between biogenic CH4 from sewer gas and thermogenic CH4 from leaking natural gas pipelines and measured CH4 and N2O flux rates and concentrations at sites from a previous study of street-level CH4 enhancements (77 out of 104 sites) as well as additional sites found through surveying sewer grates and utility manholes (27 out of 104 sites). The average isotopic signatures for δ13C-CH4 and δ2H-CH4 were −48.5‰ ± 6.0‰ and −302‰ ± 142‰. The measured flux rates ranged from 0.0 to 282.5 mg CH4 day−1 and 0.0–14.1 mg N2O day−1 (n = 43). The average CH4 and N2O concentrations measured in our study were 4.0 ± 7.6 ppm and 392 ± 158 ppb, respectively (n = 104). 72% of sites where fluxes were measured were a source of biogenic CH4. Overall, 47% of the sampled sites had biogenic CH4, while only 13% of our sites had solely thermogenic CH4. The other sites were either a source of both biogenic and thermogenic CH4 (13%), and a relatively large portion of sites had an unresolved source (29%). Overall, this survey of emissions across a large urban area indicates that production and emission of biogenic CH4 and N2O is considerable, although CH4 fluxes are lower than those reported for cities with leaky natural gas distribution systems.

At present, the majority of investigations concerning nanotoxicology in the nematode C. elegans address short-term effects. While this approach allows for the identification of uptake pathways, exposition and acute toxicity, nanoparticle-organism interactions that manifest later in the adult life of C. elegans are missed. Here we show that a microhabitat composed of liquid S-medium and live bacteria in microtiter wells prolongs C. elegans longevity and is optimally suited to monitor chronic eNP-effects over the entire life span (about 34 days) of the nematode. Silver (Ag) nanoparticles reduced C. elegans life span in concentrations ≥10 μg/mL, whereas nano ZnO and CeO₂ (1–160 μg/mL) had no effect on longevity. Monitoring of locomotion behaviors throughout the entire life span of C. elegans showed that Ag NPs accelerate the age-associated decline of swimming and increase of uncoordinated movements at concentrations of ≥10 μg/mL, whereas neuromuscular defects did not occur in response to ZnO and CeO₂ NPs. By means of a fluorescing reporter worm expressing tryptophan hydroxylase-1::DsRed Ag NP-induced behavioral defects were correlated to axonal protein aggregation and neurodegeneration in single serotonergic HSN as well as sensory ADF neurons. Notably, serotonergic ADF neurons represented a sensitive target for Ag NPs in comparison to GABAergic neurons that showed no signs of degeneration under the same conditions. We conclude that due to its analogy to the jellylike boom culture of C. elegans on microbe-rich rotting plant material liquid S-medium culture in spatially confined microtiter wells represents a relevant as well as practical tool for comparative identification of age-resolved nanoparticle effects and vulnerabilities in a significant target organism. Consistent with this, specifically middle-aged nematodes showed premature neuromuscular defects after Ag NP-exposure.

Particulate matter 2.5 (PM₂.₅) exposures during pregnancy could lead to declined birth weight, intrauterine developmental restriction, and premature delivery, however, the underlying mechanisms are still not elucidated. There are few studies concerning the effects of PM₂.₅ exposure on maternal and child health in Xi'an (one of the cities with severe air pollution of PM₂.₅ in North China). Then, this study aimed to investigate the effect of PM₂.₅ exposure in Xi'an on the offspring birth weights and the possibly associated epigenetic mechanisms. We found the Low and High groups: the offspring with declined birth weights; the decreased mRNA and protein expression of the estrogen receptor (ERs) and eNOs in the uterus; the decreased endometria vascular diameter maximum (EVDM); the increased mRNA and protein expressions of the DNMT1 and 3b in the uterus; the elevated methylation levels of the CpG sites in the CpG island of ERα promoter region in the uterus. However, no differences were observed in the mRNA or protein expressions of ERβ and DNMT3a between the Clean and PM₂.₅ exposure groups, as well as endometriavascular density (EVD). Additionally, PM₂.₅ level was negatively correlated with the ERα protein expression, EVDM and offspring birth weight, as well as the methylation level of the CpG sites in the CpG island of ERα promoter region and the ERα protein expression in the uterus; whereas the ERα protein expression was positively correlated with the offspring birth weight, as well as PM₂.₅ level and the methylation level of the CpG sites in the CpG island of ERα promoter region in the uterus. Taken together, elevated methylation level of the CpG sites in the CpG island of ERα promoter region reduces ERα expression in the uterus, which could be one of the epigenetic mechanisms that pregnant PM₂.₅ exposure reduces the offspring birth weights.

Macroalgal beds provide important habitat structure and support primary production for rocky reef communities, but are increasingly degraded as a result of human pressures. Various sources of pollution can have both direct and interactive effects on stressed ecosystems. In particular, interactions involving invertebrate grazers could potentially weaken or strengthen the overall impact of pollution on macroalgal beds. Using a paired impact-control experimental design, we tested the effects of multiple pollution sources (fish farms, marinas, sewerage, and stormwater) on translocated and locally established algal assemblages, while also considering the influence of invertebrate grazers. Marinas directly affected algal assemblages and also reduced densities of amphipods and other invertebrate mesograzers. Fish farms and sewerage outfalls tended to directly increase local establishment of foliose and leathery algae without any indication of changes in herbivory. Overall, pollution impacts on algae did not appear to be strongly mediated by changes in grazer abundance. Instead, mesograzer abundance was closely linked to availability of more complex algal forms, with populations likely to decline concurrently with loss of complex algal habitats. Macrograzers, such as sea urchins, showed no signs of a negative impact from any pollution source; hence, the influence of this group on algal dynamics is probably persistent and independent of moderate pollution levels, potentially adding to the direct impacts of pollution on algal beds in urbanised environments.

Di-2-ethylhexyl phthalate (DEHP) has been widely used as a plasticizer in industry. DEHP can cause testicular atrophy, yet the exact mechanism remains unclear. In this study, male mice were intragastrically (i.g.) administered with 0, 100, 200 or 400 mg DEHP/kg/day for 21 days. We found that DEHP caused disintegration of the germinal epithelium and decreased sperm density in the epididymis. Furthermore, there was a significant increase in the levels of cleaved Caspase-8, cleaved Caspase-3 and Bax proteins and a decrease in Bcl2 protein. The results indicated that DEHP could induce apoptosis of the testis tissue. Meanwhile, DEHP significantly induced autophagy in the testis tissues with increases in LC3-II, Atg5 and Beclin-1 proteins. The serum testosterone concentration decreased in the DEHP-treated group, implying that DEHP might lead to Leydig cell damage. Furthermore, oxidative stress was induced by DEHP in the testis. To further investigate the potential mechanism, mouse TM3 Leydig cells were treated with 0–80 μM DEHP for 48 h. DEHP significantly inhibited cell viability and induced cell apoptosis. Oxidative stress was involved in DEHP-induced apoptosis as N-Acetyl-L-cysteine (NAC), an inhibitor of oxidative stress, could rescue the inhibition of cell viability and induction of apoptosis by DEHP. Similar to the in vivo findings, DEHP could also induce cell autophagy. However, inhibition of autophagy by 3-Methyladenine (3-MA) significantly increased cell viability and inhibited apoptosis. Taken together, oxidative stress was involved in DEHP-induced apoptosis and autophagy of mouse TM3 Leydig cells, and autophagy might play a cytotoxic role in DEHP-induced cell apoptosis.