Low Exposure Concentrations Research Articles

The effect of TiO2 nanoparticles on sulfate-reducing bacteria and their consortium under anaerobic conditions

Sulfate-reducing bacteria are one of the most commonly occurring strains in industrial and waste water samples. TiO2 NPs (titanium dioxide nanoparticles) are an important component of cosmetics and toothpastes and are also useful agents as disinfectants in treatment of wastewater. The study delineates the effect of TiO2 NPs on sulfate-reducing bacteria (Desulphovibrio desulfuricans and Desulfotomaculum nigrificans) and their consortium. The specific growth of these bacteria under UVA, visible light, and dark was found to be exposure dependent. With an increase in the concentration of TiO2 NPs, insignificant changes were observed in the sulfate reduction rate. The specific growth rate of bacteria was reduced upon exposure of 1μg/mL of TiO2, whereas lower concentrations did not have any significant impact. The exopolymer release, which is indicative of the bacterial defense response, demonstrated a nanoparticle exposure-dependent increase over time, and it was significantly higher in the consortium as compared to individual strains. Similarly, the biofilm thickness and density showed a linear dependence on the NP exposure time. The surface chemical changes of exopolymers were analyzed with help of FT-IR analysis. Distortion of the consortium cells embedded within the biofilm matrix when exposed with the highest exposure dose of NPs and UV was prominent as compared to control cells. The consortium demonstrated enhanced ability to counter stress under all the experimental conditions as compared with the single bacterial strains. The sulfate-reducing potency of these bacteria under low exposure concentrations of TiO2 NPs could be used as a bioremediation tool in wastewater treatment plants.

Discovery of a low-systemic-exposure DGAT-1 inhibitor with a picolinoylpyrrolidine-2-carboxylic acid moiety

A series of diacylglycerol O-acyltransferase 1 (DGAT-1) inhibitors with a picolinoylpyrrolidine-2-carboxylic acid moiety were designed and synthesized. Of these compounds, compound 22 exhibited excellent DGAT-1-inhibitory activity (hDGAT-1 enzyme assay, 50% inhibitory concentration [IC50]=3.5±0.9nM) and effectively reduced the intracellular triglyceride contents in 3T3-L1, HepG2 and Caco-2 cells. A preliminary study of the plasma and tissue distributions of compound 22 in mice revealed low plasma exposure and high concentrations in different segments of the intestine and liver, which may facilitate targeting DGAT-1. Furthermore, in an acute lipid challenge test, compound 22 showed a dose-dependent inhibitory effect on high-serum triglycerides in C57/KSJ mice induced by olive oil (1, 3, and 10mg/kg, i.g.).

Hazard assessment of nickel nanoparticles in soil-The use of a full life cycle test with Enchytraeus crypticus.

Nanoparticles (NPs) such as nickel (Ni) are widely used in several applications. Nevertheless, the environmental effects of Ni NPs are still poorly understood. In the present study, the toxicity of Ni NPs and nickel nitrate (NiNO3 ) was assessed using the standard test species in soil ecotoxicology, Enchytraeus crypticus (Oligochaeta), in a full life cycle test, adding the endpoints hatching, growth, and time to reach maturity, besides survival and reproduction as in the standard Organisation for Economic Co-operation and Development Guideline 220 and/or International Organization for Standardization 16387. For Ni NPs, the Ni in soil and in soil solution was concentration- and time-dependent, with a relatively higher soil solution content in the lower and shorter exposure concentrations and times. Overall, NiNO3 was more toxic than Ni NPs, and toxicity seemed to occur via different mechanisms. The former caused reduced hatching (50% effect concentration [EC50] = 39 mg Ni/kg soil), and the negative effects remained throughout the life cycle, in all measured endpoints (growth, maturation, survival, and reproduction). For Ni NPs, hatching was the most sensitive endpoint (EC50 = 870 mg Ni/kg soil), although the organisms recovered; that is, additional endpoints across the life cycle showed that this effect corresponded to a delay in hatching because organisms survived and reproduced at concentrations up to 1800 mg Ni/kg soil. On the other hand, the lowest tested concentration of Ni NPs (100 mg Ni/kg soil) caused reproduction effects similar to those at higher concentrations (1000 and 1800 mg Ni/kg soil). The present results show that the potential implications of a nonmonotonic dose response should be considered when assessing the risks of Ni NP exposure in soil. Environ Toxicol Chem 2017;36:2934-2941. © 2017 SETAC.

Graphene oxide nanosheets induce DNA damage and activate the base excision repair (BER) signaling pathway both in vitro and in vivo

Graphene oxide (GO) has widespread concerns in the fields of biological sciences and medical applications. Currently, studies have reported that excessive GO exposure can cause cellular DNA damage through reactive oxygen species (ROS) generation. However, DNA damage mediated response of the base excision repair (BER) pathway due to GO exposure is not elucidated yet. Therefore, we exposed HEK293T cells and zebrafish embryos to different concentrations of GO for 24 h, and transcriptional profiles of BER pathway genes, DNA damage, and cell viability were analyzed both in vitro and in vivo. Moreover, the deformation of HEK293T cells before and after GO exposure was also investigated using atomic force microscopy (AFM) to identify the physical changes occurred in the cells' structure. CCK-8 and Comet assay revealed the significant decrease in cell viability and increase in DNA damage in HEK293T cells at higher GO doses (25 and 50 μg/mL). Among the investigated genetic markers in HEK293T cells, BER pathway genes (APEX1, OGG1, CREB1, UNG) were significantly up-regulated upon exposure to higher GO dose (50 μg/mL), however, low exposure concentration (5, 25 μg/mL) failed to induce significant genetic induction except for CREB1 at 25 μg/mL. Additionally, the viscosity of HEK293T cells decreased upon GO exposure. In zebrafish, the results of up-regulated gene expressions (apex1, ogg1, polb, creb1) were consistent with those in the HEK293T cells. Taken all together, the exposure to elevated GO concentration could cause DNA damage to HEK293T cells and zebrafish embryos; BER pathway could be proposed as the possible inner response mechanism.

Exposure to Deepwater Horizon oil and Corexit 9500 at low concentrations induces transcriptional changes and alters immune transcriptional pathways in sheepshead minnows

The 2010 Deepwater Horizon (DWH) oil spill caused the release of 4.9 million barrels of crude oil into the Gulf of Mexico, followed by the application of 2.9 million L of the dispersant, Corexit™ to mitigate the spread of oil. The spill resulted in substantial shoreline oiling, potentially exposing coastal organisms to polyaromatic hydrocarbon (PAH) and dispersant contaminants. To investigate molecular effects in fish following exposure to environmentally relevant concentrations of DWH oil and dispersants, we exposed adult sheepshead minnows (Cyprinodon variegatus) to two concentrations of high-energy water-accommodated fraction (HEWAF), chemically enhanced water-accommodated fraction (CEWAF) or Corexit 9500™ for 7 and 14days. Resulting changes in hepatic gene expression were measured using 8×15K microarrays. Analytical chemistry confirmed PAH concentrations in HEWAF and CEWAF treatments were low (ranging from 0.26 to 5.98μg/L), and likely representative of post-spill environmental concentrations. We observed significant changes to gene expression in all treatments (relative to controls), with Corexit and CEWAF having a greater effect on expression patterns in the liver than HEWAF treatments. Sub-network enrichment analysis of biological pathways revealed that the greatest number of altered pathways in high dose HEWAF and CEWAF treatments occurred following a 7-day exposure. Pathways related to immunity comprised the majority of pathways affected in each treatment, followed by pathways related to blood and circulation processes. Our results indicate that oil composition, concentration, and exposure duration all affect molecular responses in exposed fish, and suggest that low-concentration exposures may result in sub-lethal adverse effects.

Short-term exposure to gold nanoparticle suspension impairs swimming behavior in a widespread calanoid copepod

Calanoid copepods play an important role in the functioning of marine and brackish ecosystems. Information is scarce on the behavioral toxicity of engineered nanoparticles to these abundant planktonic organisms. We assessed the effects of short-term exposure to nonfunctionalized gold nanoparticles on the swimming behavior of the widespread estuarine copepod Eurytemora affinis. By means of three-dimensional particle tracking velocimetry, we reconstructed the trajectories of males, ovigerous and non-ovigerous females. We quantified changes in their swimming activity and in the kinematics and geometrical properties of their motion, three important descriptors of the motility patterns of zooplankters. In females, exposure to gold nanoparticles in suspension (11.4 μg L−1) for 30 min caused depressed activity and lower velocity and acceleration, whereas the same exposure caused minimal effects in males. This response differs clearly from the hyperactive behavior that is commonly observed in zooplankters exposed to pollutants, and from the generally lower sensitivity of female copepods to toxicants. Accumulation of gold nanoparticles on the external appendages was not observed, precluding mechanical effects. Only very few nanoparticles appeared sporadically in the inner part of the gut in some samples, either as aggregates or as isolated nanoparticles, which does not suggest systemic toxicity resulting from pronounced ingestion. Hence, the precise mechanisms underlying the behavioral toxicity observed here remain to be elucidated. These results demonstrate that gold nanoparticles can induce marked behavioral alterations at very low concentration and short exposure duration. They illustrate the applicability of swimming behavior as a suitable and sensitive endpoint for investigating the toxicity of nanomaterials present in estuarine and marine environments. Changes in swimming behavior may impair the ability of planktonic copepods to interact with their environment and with other organisms, with possible impacts on population dynamics and community structure.

Dualistic immunomodulation of sub-chronic microcystin-LR exposure on the innate-immune defense system in male zebrafish

Microcystins (MCs), produced by toxic cyanobacterial blooms that appeared world wildly in eutrophication waters, have often caused fish illness and even massive death cases. Among at least 90 structural variants, microcystin-LR (MC-LR) is the most common and toxic variant. In order to better understand innate immune responses in fish disrupted by environmental concentrations of MC-LR, male zebrafish (Danio rerio) were exposed to 0, 0.3, 1, 3, 10 and 30 μg/L MC-LR for 30 d, and the changes in splenic pathology and immunological gene expression as well as serum immune parameters were studied. In the low concentration groups (0.3, 1 and 3 μg/L), zebrafish displayed splenic inflammatory changes including the formation of melano-macrophage centers and the increase of macrophage pseudopodia, remarkable elevation of serum C3 levels, and significantly upregulated expression of innate immune-related genes (c3b, lyz, il1β, tnfα and ifnγ). In contrast, high concentrations of MC-LR (10 and 30 μg/L) resulted in the degeneration of splenic lymphocytes and macrophages, and down-regulation of immune-related genes as well as significant decreases in the level of serum C3. Furthermore, significant increases in the activity of serum ACP and ALP suggested that high concentrations of MC-LR increased permeability of macrophage plasma membrane or cellular necrosis, and subsequently decreased innate immune function. Our findings illustrated that sub-chronic exposure of MC-LR has dualistic influences on fish innate immune system with inflammatory activation at low exposure concentrations but turned to immune inhibition with the increases of exposure concentration.

Transcriptome analysis of the brain of the sea bream (Sparus aurata) after exposure to human pharmaceuticals at realistic environmental concentrations

Human pharmaceuticals such as Acetaminophen, Atenolol and Carbamazepine are pseudo persistent aquatic pollutants with yet unknown sub-lethal effects at environmentally relevant concentrations. Gilthead seabream (Sparus aurata) were exposed to Acetaminophen: 31.90 ± 11.07 μg L−1; Atenolol: 0.95 ± 0.38 μg L−1 and Carbamazepine: 6.95 ± 0.13 μg L−1 in a 28 day flow through experiment to (1) determine whether exposure to low concentrations in the μg·L−1 range of the pharmaceuticals alters the brain transcriptome and, (2) identify different expression profiles and treatment specific modes of action and pathways. Despite low exposure concentrations, 411, 7 and 612 differently expressed transcripts were identified in the individual treatments with Acetaminophen, Atenolol and Carbamazepine, respectively. Functional analyses of differentially expressed genes revealed a significant over representation of several biological processes, cellular compartment features and molecular functions for both Acetaminophen and Carbamazepine treatments. Overall, the results obtained in seabream brain suggest similar physiological responses to those observed in humans also at environmental concentrations, as well as the existence of treatment specific processes that may be useful for the development of biomarkers of contamination.

Sorafenib and 2,3,5-triiodobenzoic acid-loaded imageable microspheres for transarterial embolization of a liver tumor

Sorafenib (SOF; an angiogenesis inhibitor) and 2,3,5-triiodobenzoic acid (TIBA; a contrast agent for computed tomography imaging)-loaded poly(lactic-co-glycolic acid) (PLGA) microspheres (MSs) were fabricated. Embolization, drug delivery, and tracing the distribution of MSs for liver cancer therapy were accomplished with the developed MSs after their intra-arterial (IA) administration. SOF/TIBA/PLGA MSs with 24.8–28.5 µm mean diameters were prepared, and the sustained release of SOF from MSs was observed. Lower systemic exposure (represented as the area under the curve [AUC]) and maximum drug concentration in plasma (Cmax) values of the SOF/TIBA/PLGA MSs group (IA administration, 1 mg/kg) in the results of the pharmacokinetic study imply alleviated unwanted systemic effects (e.g., hand and foot syndrome), compared to the SOF solution group (oral administration, 10 mg/kg). In a rat hepatoma model, the increase of microvessel density (MVD) following arterial embolization (i.e., reactive angiogenesis) was partially limited by SOF/TIBA/PLGA MSs. This resulted in the SOF/TIBA/PLGA MSs group (IA administration, single dosing, 1 mg/kg) showing a smaller tumor size increase and viable tumor portion compared to the TIBA/PLGA MSs group. These findings suggest that a developed SOF/TIBA/PLGA MS can be a promising therapeutic system for liver cancer using a transarterial embolization strategy.

Effects of polystyrene microplastics on the fitness of earthworms in an agricultural soil

Microplastics (MPs) pollution is widespread in the environment, while the effects of MPs on the soil organisms are poorly understood. In this study, we investigated the fitness of earthworms (E. Foetida) exposed to MPs (Polystyrene, 58 μm) in soils at the concentrations of 0, 0.25, 0.5, 1 and 2% (w/w). The results showed that MPs had little effects on the fitness of earthworms under low exposure concentrations (≤ 0.5 % (w/w)), while MPs exposure with high concentrations (i.e., 1% and 2%) significantly inhibited the growth and increased the mortality of earthworms. The results indicated that the MPs pollution in soils have an adverse effect on the fitness of soil organisms, and implied the ecological risk of MPs in terrestrial ecosystems.

Histological changes, lipid metabolism and oxidative stress in the liver of Bufo gargarizans exposed to cadmium concentrations

Chinese toad (Bufo gargarizans) were exposed to different concentrations of cadmium (5, 50, 100, 200 and 500μg Cd L-1) from Gosner stage 3-42. Metamorphosis rate, body weight, total length and body length were measured. Histological alterations in thyroid gland and liver were examined. Changes in hepatocyte were also examined using Transmission electron microscopic. In addition, the mRNA expression of several genes involved in lipid metabolism, oxidative stress and thyroid hormones signaling pathways were also measured. Our results showed that 200 and 500μg Cd L-1 decreased the metamorphosis rate and inhibited the body size of B.gargarizans larvae at G42. Moreover, histological examinations have clearly exhibited that cadmium caused liver damage. Ultrastructural examination revealed lipid accumulation and abnormal mitochondria. Exposure to 200 and 500μg Cd L-1 significantly up-regulated mRNA expression of D2, SOD, GPx, ACC and FAE, but down-regulated mRNA expression of TRα, TRβ, PPARα, ACOX, CPT and SCP. However, low Cd concentration (5, 50 and 100) exposure did not cause any effect in genes expression. Thus, we conclude that high Cd concentrations could affect the normal processes of lipid metabolism though increasing lipid synthesis and reducing the ability of fatty acid β-oxidation, and disturb thyroid hormone pathways in liver, and induced oxidative stress. In addition, lipid metabolism might be regulated by THs. To our knowledge, the present study is the first to report the influence of cadmium on hepatic lipid metabolism in B.gargarizans and will greatly provide new insights into cadmium hepatotoxicity in amphibian.

Silica Cross-Linked Micellar Core–Shell Nanoparticles Encapsulating IR-780 with Strong Bright and Good Biocompatibility for Optical Imaging In Vivo

IR-780 iodide, a near-infrared (NIR) fluorescent heptamethine dye, has attracted wide attention in the biomedical community. However, hydrophobicity and toxicity severely limit its further biomedical application. Although many successful efforts have been made to increase its solubility and biocompatibility, a strong fluorescent signal and longer retention time are in high demand in biomedical application in vivo as well as basic science research. In this work, we report the development of novel silica cross-linked micellar core–shell nanoparticles encapsulating IR-780 (NIR-Silica NPs) and their utility for biomedical imaging in vivo. Compared to free IR-780, the solubility of NIR-Silica NPs was not only greatly increased, but there was also a dramatic 5–7-fold enhancement of fluorescence intensity. More importantly, the exceptionally small size (25 nm) and colloidal stability of the NPs are also sufficient to realize the enhanced permeability and retention effect. In vitro cell viability assays further indicated that the NIR-Silica NPs are safer even at the highest concentration tested of 1.0 mg/mL. Finally, sentinel lymph node mapping and long-term tumor imaging in vivo demonstrated that the NIR-Silica NPs have a long circulation time and higher signal-to-noise ratio at a very low dye concentration and short exposure time (0.2 s). Therefore, the NIR-Silica NPs may be a promising fluorescence imaging agent for clinical application.

Life-cycle exposure of fathead minnows to environmentally relevant concentrations of the β-blocker drug propranolol.

Propranolol is a human pharmaceutical β-blocker that has been detected in municipal wastewater effluents at ng/L to low μg/L. To assess the potential of this compound to affect fish, fathead minnow (Pimephales promelas) were exposed for a life cycle in a flow-through system to nominal propranolol concentrations of 0.87 ng/L, 8.7 ng/L, 87 ng/L, 870 ng/L, and 8700 ng/L. Measured propranolol concentrations were below detection for the 2 lowest exposure concentrations, and were 76 ng/L, 580 ng/L, and 7800 ng/L for the 3 highest exposure concentrations. During the 162-d to 165-d exposure, no significant changes in weights or lengths were seen in fathead minnows, although the highest concentration of propranolol did cause a 15% decrease in survival of larval and juvenile stage fish compared with controls. At maturity, there were no significant changes in condition factor, liver-somatic index, or secondary sex characteristics in propranolol-exposed male or female fish. Female gonadosomatic index was significantly decreased in fish exposed to the highest concentrations of propranolol, probably because of increased egg-laying. Fathead minnows from all propranolol exposures produced more eggs than control fish, with fish exposed to 7800 ng/L propranolol producing 70% more eggs per female (p = 0.060), and having significantly increased clutch size (p = 0.008). Egg quality, % fertilization, % hatching, and % deformities in F1 fry were unaffected by propranolol exposure of fish. Propranolol exposure caused no effects in fathead minnows, except at the highest exposure concentration (7800 ng/L), where there were slight decreases in survival of juvenile minnows, and indications of increased reproduction. The present study is important because it is the first to assess the potential for effects in fish exposed to propranolol for a life cycle. Environ Toxicol Chem 2017;36:1644-1651. © 2016 SETAC.

The effects of emodin on cell viability, respiratory burst and gene expression of Nrf2-Keap1 signaling molecules in the peripheral blood leukocytes of blunt snout bream (Megalobrama amblycephala)

We determined the effects of emodin on the cell viability, respiratory burst activity, mRNA levels of antioxidative enzymes (Cu-Zn SOD, CAT and NOX2), and gene expressions of the Nrf2-Keap1 signaling molecules in the peripheral blood leukocytes of blunt snout bream. Triplicate groups of cultured cells were treated with different concentrations of emodin (0.04–25 μg/ml) for 24 h. Results showed that the emodin caused a dramatic loss in cell viability, and occurred in a dose-dependent manner. Emodin exposure (1–25 μg/ml) were significantly induced the ROS generation compared to the control. The respiratory burst and NADPH oxidase activities were significantly induced at a concentration of 0.20 μg/ml, and inhibited at 25 μg/ml. Besides, mRNA levels of antioxidant enzyme genes were dramatically regulated by emodin exposure for 24 h. During low concentrations of exposure, mRNA levels of Cu-Zn SOD in the cells treated with 0.04, 0.20 μg/ml, CAT, NOX2 and Nrf2 in the cells treated with 1 μg/ml were sharply increased, respectively. Whereas, high concentrations were dramatically down-regulated the gene expressions of CAT in the cells treated with 5, 25 μg/ml and NOX2 in the cells treated with 25 μg/ml. Furthermore, sharp increase in Keap1and Bach1 expression levels were observed a dose-dependent manner. In conclusion, this study demonstrated that emodin could induce antioxidant defenses which were involved in cytotoxic activities, respiratory burst and the transcriptional regulation levels of antioxidant enzymes and Nrf2-Keap1 signaling molecules.

Combined toxic effects and mechanisms of microsystin-LR and copper on Vallisneria Natans (Lour.) Hara seedlings

Microcystin-LR (MCLR) and copper are commonly found in eutrophic water bodies because of eutrophic run-offs, cyanobacterial blooms, and copper algicide applications. However, the ecotoxicological risk of their combination remains unknown. This study investigated the effect of MCLR, Cu, and their mixture on the growth and physiological responses of Vallisneria natans. Results showed that the combined toxicity of them was concentration dependent. Synergistic effects were elicited at low concentrations of MCLR and Cu exposure (≤0.25+0.64mg/L). Additive or antagonistic effects were induced at higher concentrations. Single and combined exposures could induce oxidative stress, such as increased superoxide anion radical levels. To cope with oxidative stress, V. natans could activate their antioxidant defense systems, such as enhanced superoxide dismutase production and changes in peroxidase activities. Exposure to combined MCLR and Cu (even only with 0.005+0.041mg/L) adversely affected their antioxidant defense systems. As a consequence, malondialdehyde levels significantly increased. The interaction of MCLR and Cu could also significantly increase the bioaccumulations of MCLR and Cu. This increase could be accounted for their synergistic toxic effects on V. natans. Our results suggested that the exacerbated ecological hazard of MCLR and Cu with environmental concentrations may harm aquatic ecosystems.

Blood cadmium concentrations and environmental exposure sources in newcomer South and East Asian women in the Greater Toronto Area, Canada

BackgroundImmigrant women are often identified as being particularly vulnerable to environmental exposures and health effects. The availability of biomonitoring data on newcomers is limited, thus, presenting a challenge to public health practitioners in the identification of priorities for intervention. ObjectivesIn fulfillment of data needs, the purpose of this study was to characterize blood concentrations of cadmium (Cd) among newcomer women of reproductive age (19–45 years of age) living in the Greater Toronto Area (GTA), Canada and to assess potential sources of environmental exposures. MethodsA community-based model, engaging peer researchers from the communities of interest, was used for recruitment and follow-up purposes. Blood samples were taken from a total of 211 newcomer women from South and East Asia, representing primary, regional origins of immigrants to the GTA, and environmental exposure sources were assessed via telephone survey. Metal concentrations were measured in blood samples (diluted with 0.5% (v/v) ammonium hydroxide and 0.1% (v/v) octylphenol ethoxylate) using a quadrupole ICP-MS. Survey questions addressed a wide range of environmental exposure sources, including dietary and smoking patterns and use of nutritional supplements, herbal products and cosmetics. ResultsA geometric mean (GM) blood Cd concentration of 0.39µg/L (SD:±2.07µg/L) was determined for study participants (min/max: <0.045µg/L (LOD)/2.36µg/L). Several variables including low educational attainment (Relative Ratio (RR) (adjusted)=1.50; 95% CI 1.17–1.91), milk consumption (RR (adjusted)=0.86; 95% CI 0.76–0.97), and use of zinc supplements (RR (adjusted)=0.76; 95% CI 0.64–0.95) were observed to be significantly associated with blood Cd concentrations in the adjusted regression model. The variable domains socioeconomic status (R2adj=0.11) and country of origin (R2adj=0.236) were the strongest predictors of blood Cd. ConclusionBlood Cd concentrations fell below those generally considered to be of human health concern. However, negative health effects cannot be entirely excluded, especially for those that fall in the upper percentile range of the distribution, given the mounting evidence for negative health outcomes at low environmental exposure concentrations.

Synthesis of Cationized Magnetoferritin for Ultra-fast Magnetization of Cells.

Many important biomedical applications, such as cell imaging and remote manipulation, can be achieved by labeling cells with superparamagnetic iron oxide nanoparticles (SPIONs). Achieving sufficient cellular uptake of SPIONs is a challenge that has traditionally been met by exposing cells to elevated concentrations of SPIONs or by prolonging exposure times (up to 72 hr). However, these strategies are likely to mediate toxicity. Here, we present the synthesis of the protein-based SPION magnetoferritin as well as a facile surface functionalization protocol that enables rapid cell magnetization using low exposure concentrations. The SPION core of magnetoferritin consists of cobalt-doped iron oxide with an average particle diameter of 8.2 nm mineralized inside the cavity of horse spleen apo-ferritin. Chemical cationization of magnetoferritin produced a novel, highly membrane-active SPION that magnetized human mesenchymal stem cells (hMSCs) using incubation times as short as one minute and iron concentrations as lows as 0.2 mM.

Synthesis of Cationized Magnetoferritin for Ultra-fast Magnetization of Cells

Many important biomedical applications, such as cell imaging and remote manipulation, can be achieved by labeling cells with superparamagnetic iron oxide nanoparticles (SPIONs). Achieving sufficient cellular uptake of SPIONs is a challenge that has traditionally been met by exposing cells to elevated concentrations of SPIONs or by prolonging exposure times (up to 72 hr). However, these strategies are likely to mediate toxicity. Here, we present the synthesis of the protein-based SPION magnetoferritin as well as a facile surface functionalization protocol that enables rapid cell magnetization using low exposure concentrations. The SPION core of magnetoferritin consists of cobalt-doped iron oxide with an average particle diameter of 8.2 nm mineralized inside the cavity of horse spleen apo-ferritin. Chemical cationization of magnetoferritin produced a novel, highly membrane-active SPION that magnetized human mesenchymal stem cells (hMSCs) using incubation times as short as one minute and iron concentrations as lows as 0.2 mM.

Exposure to SSRI-type antidepressants increases righting time in the marine snail Ilyanassa obsoleta.

Exposure to human antidepressants has been shown to disrupt locomotion and other foot-mediated mechanisms in aquatic snails. We tested the effect of three selective serotonin reuptake inhibitor (SSRI)- and one selective serotonin-norepinephrine reuptake inhibitor (SNRI)-type antidepressants on the righting response in the marine snail, Ilyanassa obsoleta. All four antidepressants (fluoxetine, sertraline, paroxetine, venlafaxine) significantly increased righting time compared with controls with an exposure time as short as 1h. Dose responses were nonmonotonic with effects seen mainly at the lowest exposure concentrations and shortest duration. The lowest concentration to show an effect was 3.45μg/L fluoxetine with a 2-h exposure period and is about 3.71 times higher than environmental concentrations. Our results highlight rapid disruption of another foot-mediated behavior in aquatic snails by SSRI-type antidepressants. We discuss these and other reported nonmonotonic dose responses caused by antidepressants in terms of the various possible physiological mechanisms of action in nontarget aquatic species.

Effects of glufosinate on the growth of and microcystin production by Microcystis aeruginosa at environmentally relevant concentrations

Harmful algal blooms (HABs) have been emerging as a worldwide issue due to their detrimental effect to water quality and the threat to ecological health. However, there were scarcely reports on whether existing agrochemicals such as herbicides have potential effects on Microcystis aeruginosa (M. aeruginosa) which may form large surface blooms. In this study, we aimed to demonstrate the effects of glufosinate, a widely use herbicide in the world, on the growth of M. aeruginosa. The change of the content of intracellular (intra-) and extracellular (extra-) levels of microcystin-LR (MC-LR) were also determined by HPLC. The mRNA level of mcyA, mcyD, mcyH related to the production of MC-LR was detected after 48h exposure to glufosinate. Our results revealed that low concentrations of glufosinate exposure (0.5mg/L, 1mg/L) would promote the growth of M. aeruginosa. It was worth noting intra-MC-LR contents of algal cells were also significantly increased at low concentrations of glufosinate exposure (1mg/L). While at high concentrations (5mg/L, 10mg/L), glufosinate could induce the MDA level and inhibit the growth of M. aeruginosa that would limit the production of MC-LR to the water body. At last, the transcription levels of algae toxin synthesis related genes mcyA and mcyD were increased significantly at environmentally relevant concentrations of glufosinate, which may affect the MC production. This study not only illuminated effects of glufosinate on growth of and MC-LR synthesis of M. aeruginosa at environmentally relevant concentrations, but also reminding us the potential risk caused by herbicide use should arouse concerns.