2018 State-of the Science of Dispersants and Dispersed Oil (DDO) in U.S. Arctic Waters: Eco-Toxicity and Sublethal Impacts

Chemical dispersants were employed on an unprecedented scale during the Deepwater Horizon oil spill in the Gulf of Mexico, and could be a response option should a large spill occur in Arctic waters. The use of dispersants in response to that spill raised concerns regarding the need for chemical dispersants, the fate of the oil and dispersants, and their potential impacts on human health and the environment. Concerns remain that would be more evident in the Arctic, where the remoteness and harsh environmental conditions would make a response to any oil spill very difficult. An outcome of a 2013 Arctic oil spill exercise for senior federal agency leadership identified the need for an evaluation of the state-of-the-science of dispersants and dispersed oil (DDO), and a clear delineation of the associated uncertainties that remain, particularly as they apply to Arctic waters. The National Oceanic and Atmospheric Administration (NOAA), in partnership with the Coastal Response Research Center (CRRC), and in consultation with the U.S. Environmental Protection Agency (EPA) embarked on a project to seek expert review and evaluation of the state-of-the-science and the uncertainties involving DDO. The project focused on five areas and how they might be affected by Arctic conditions: dispersant effectiveness, distribution and fate, transport and chemical behavior, environmental impacts, and public health and safety. This publication (1 of 5) addresses efficacy and effectiveness

Developmental toxicity of bisphenol A diglycidyl ether (epoxide resin badge) during the early life cycle of a native amphibian species

Bisphenol A diglycidyl ether (BADGE) is used in packaging materials, in epoxy adhesives, and as an additive for plastics, but it is also a potential industrial wastewater contaminant. The aim of the present study was to evaluate the adverse effects of BADGE on Rhinella arenarum by means of standardized bioassays at embryo–larval development. The results showed that BADGE was more toxic to embryos than to larvae at all exposure times. At acute exposure, lethality rates of embryos exposed to concentrations of 0.0005 mg/L BADGE and greater were significantly higher than rates in the vehicle control, whereas lethality rates of larvae were significantly higher in concentrations of 10 mg/L BADGE and greater. The toxicity then increased significantly, with 96‐h median lethal concentrations (LC50s) of 0.13 mg/L and 6.9 mg/L BADGE for embryos and larvae, respectively. By the end of the chronic period, the 336‐h LC50s were 0.04 mg/L and 2.2 mg/L BADGE for embryos and larvae, respectively. This differential sensitivity was also ascertained by the 24‐h pulse exposure experiments, in which embryos showed a stage‐dependent toxicity, with blastula being the most sensitive stage and S.23 the most resistant. The most important sublethal effects in embryos were cell dissociation and delayed development, whereas the main abnormalities observed in larvae related to neurotoxicity, as scare response to stimuli and narcotic effect.Fil: Hutler Wolkowicz, Ianina Ruth. Universidad Nacional de San Martín. Instituto de Investigación e Ingeniería Ambiental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Svartz, Gabriela Veronica. Universidad Nacional de San Martín. Instituto de Investigación e Ingeniería Ambiental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Aronzon, Carolina Mariel. Universidad Nacional de San Martín. Instituto de Investigación e Ingeniería Ambiental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Perez Coll, Cristina Silvia. Universidad Nacional de San Martín. Instituto de Investigación e Ingeniería Ambiental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Transcriptional responses of Biomphalaria pfeifferi and Schistosoma mansoni following exposure to niclosamide, with evidence for a synergistic effect on snails following exposure to both stressors.

BackgroundSchistosomiasis is one of the world's most common NTDs. Successful control operations often target snail vectors with the molluscicide niclosamide. Little is known about how niclosamide affects snails, including for Biomphalaria pfeifferi, the most important vector for Schistosoma mansoni in Africa. We used Illumina technology to explore how field-derived B. pfeifferi, either uninfected or harboring cercariae-producing S. mansoni sporocysts, respond to a sublethal treatment of niclosamide. This study afforded the opportunity to determine if snails respond differently to biotic or abiotic stressors, and if they reserve unique responses for when presented with both stressors in combination. We also examined how sporocysts respond when their snail host is treated with niclosamide.Principal findingsCercariae-producing sporocysts within snails treated with niclosamide express ~68% of the genes in the S. mansoni genome, as compared to 66% expressed by intramolluscan stages of S. mansoni in snails not treated with niclosamide. Niclosamide does not disable sporocysts nor does it seem to provoke from them distinctive responses associated with detoxifying a xenobiotic. For uninfected B. pfeifferi, niclosamide treatment alone increases expression of several features not up-regulated in infected snails including particular cytochrome p450s and heat shock proteins, glutathione-S-transferases, antimicrobial factors like LBP/BPI and protease inhibitors, and also provokes strong down regulation of proteases. Exposure of infected snails to niclosamide resulted in numerous up-regulated responses associated with apoptosis along with down-regulated ribosomal and defense functions, indicative of a distinctive, compromised state not achieved with either stimulus alone.Conclusions/significanceThis study helps define the transcriptomic responses of an important and under-studied schistosome vector to S. mansoni sporocysts, to niclosamide, and to both in combination. It suggests the response of S. mansoni sporocysts to niclosamide is minimal and not reflective of a distinct repertoire of genes to handle xenobiotics while in the snail host. It also offers new insights for how niclosamide affects snails

A new mathematical model for radiation cell killing mechanism: Target cumulating model

There are numerous mathematical or statistical models have been given out for radiation cell killing mechanism. Unfortunately, none of the model could explain the mechanism perfectly. The more advanced model for it is still necessary to be researched. Following common assumption, a new theoretical model named "target cumulating" model is induced from the molecular and particle physics level. The result of theoretical calculation gives the equation of cell survival rate corresponding to delivered dose and other sensitivity parameters. In addition to fit the cell survival curve well, the new model showed advantages with comparing to previous models. Also, the new model predicts or explains some phenomenon that had been observed in laboratory (e.g. dose rate effect and low dose hypersensitivity)

Guinea pigs sublethally infected with aerosolized Legionella pneumophila develop humoral and cell-mediated immune responses and are protected against lethal aerosol challenge. A model for studying host defense against lung infections caused by intracellular pathogens.

We have employed the guinea pig model of L. pneumophila infection, which mimics Legionnaires' disease in humans both clinically and pathologically, to study humoral and cell-mediated immune responses to L. pneumophila and to examine protective immunity after aerosol exposure, the natural route of infection. Guinea pigs exposed to sublethal concentrations of L. pneumophila by aerosol developed strong humoral immune responses. By the indirect fluorescent antibody assay, exposed guinea pigs had a median serum antibody titer (expressed as the reciprocal of the highest positive dilution) of 32, whereas control guinea pigs had a median titer of less than 1. Sublethally infected (immunized) guinea pigs also developed strong cell-mediated immune responses. In response to L. pneumophila antigens, splenic lymphocytes from immunized but not control animals proliferated strongly in vitro, as measured by their capacity to incorporate [3H]thymidine. Moreover, immunized but not control guinea pigs developed strong cutaneous delayed-type hypersensitivity to intradermally injected L. pneumophila antigens. Sublethally infected (immunized) guinea pigs exhibited strong protective immunity to L. pneumophila. In two independent experiments, all 22 immunized guinea pigs survived aerosol challenge with one or three times the lethal dose of L. pneumophila whereas none of 16 sham-immunized control guinea pigs survived (p less than 0.0001 in each experiment). Immunized guinea pigs were not protected significantly from challenge with 10 times the lethal dose. Immunized but not control animals cleared the bacteria from their lungs. This study demonstrates that guinea pigs sublethally infected with L. pneumophila by the aerosol route develop strong humoral immune responses to this pathogen, develop strong cell-mediated immune responses and cutaneous delayed-type hypersensitivity to L. pneumophila antigens, are protected against subsequent lethal aerosol challenge, and are able to clear the bacteria from their lungs. The guinea pig model of L. pneumophila pulmonary infection is as an excellent one for studying general principles of host defense against pulmonary infections caused by intracellular pathogens

Relations of environmental contaminants, algal toxins, and diet with the reproductive success of American alligators on Florida Lakes

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Intrathymic expression of Flt3 ligand enhances thymic recovery after irradiation

Hematopoietic stem cell transplantation (HSCT) requires conditioning treatments such as irradiation, which leads to a severely delayed recovery of T cell immunity and constitutes a major complication of this therapy. Currently, our understanding of the mechanisms regulating thymic recovery is limited. It is known that a subpopulation of bone marrow (BM)-derived thymic immigrant cells and the earliest intrathymic progenitors express the FMS-like tyrosine kinase 3 (Flt3) receptor; however, the functional significance of this expression in the thymus is not known. We used the BM transplant model to investigate the importance of Flt3 ligand (FL) for the regeneration of the T cell compartment. We show that FL is expressed in the adult mouse thymus on the surface of perivascular fibroblasts. These cells surround the proposed thymic entry site of Flt3 receptor-positive T cell progenitors. After irradiation, perivascular FL expression is up-regulated and results in an enhanced recovery of thymic cellularity. Thymic grafting experiments confirm an intrathymic requirement for FL. Collectively, these results show that thymic stromal cell-mediated FL-Flt3 receptor interactions are important in the reconstitution of thymopoiesis early after lethal irradiation and HSCT, and provide a functional relevance to the expression of the Flt3 receptor on intrathymic T cell progenitors

Acute toxicity of arsenic and oxidative stress responses in the embryonic development of the common South American toad Rhinella arenarum

Arsenic (As), a natural element of ecological relevance, is found in natural water sources throughout Argentina in concentrations between 0.01mg/L and 15mg/L. The autochthonous toad Rhinella arenarum was selected to study the acute toxicity of As and the biochemical responses elicited by the exposure to As in water during its embryonic development. The median lethal concentration (LC50) value averaged 24.3mg/L As and remained constant along the embryonic development. However, As toxicity drastically decreased when embryos were exposed from heartbeat-stage on day 4 of development, suggesting the onset of detoxification mechanisms. Given the environmental concentrations of As in Argentina, there is a probability of exceeding lethal levels at 1% of sites. Arsenic at sublethal concentrations caused a significant decrease in the total antioxidant potential but generated an increase in endogenous glutathione (GSH) content and glutathione S-transferase (GST) activity. This protective response might prevent a deeper decline in the antioxidant system and further oxidative damage. Alternatively, it might be linked to As conjugation with GSH for its excretion. The authors conclude that toad embryos are more sensitive to As during early developmental stages and that relatively high concentrations of this toxic element are required to elicit mortality, but oxidative stress may be an adverse effect at sublethal concentrations.Fil: Mardirosian, Mariana Noelia. Universidad Nacional del Comahue. Facultad de Ingeniería. Departamento de Química. Laboratorio de Investigaciones Bioquímicas, Químicas y de Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Lascano, Cecilia Ines. Universidad Nacional del Comahue. Facultad de Ingeniería. Departamento de Química. Laboratorio de Investigaciones Bioquímicas, Químicas y de Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ferrari, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto de Investigación y Desarrollo en Ingeniería de Procesos, Biotecnología y Energias Alternativas. Universidad Nacional del Comahue. Instituto de Investigación y Desarrollo en Ingeniería de Procesos, Biotecnología y Energias Alternativas; ArgentinaFil: Bongiovanni, Guillermina Azucena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto de Investigación y Desarrollo en Ingeniería de Procesos, Biotecnología y Energias Alternativas. Universidad Nacional del Comahue. Instituto de Investigación y Desarrollo en Ingeniería de Procesos, Biotecnología y Energias Alternativas; ArgentinaFil: Venturino, Andres. Universidad Nacional del Comahue. Facultad de Ingeniería. Departamento de Química. Laboratorio de Investigaciones Bioquímicas, Químicas y de Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

The MarR-Type Repressor MhqR Confers Quinone and Antimicrobial Resistance in Staphylococcus aureus

Aims: Quinone compounds are electron carriers and have antimicrobial and toxic properties due to their mode of actions as electrophiles and oxidants. However, the regulatory mechanism of quinone resistance is less well understood in the pathogen Staphylococcus aureus. Results: Methylhydroquinone (MHQ) caused a thiol-specific oxidative and electrophile stress response in the S. aureus transcriptome as revealed by the induction of the PerR, QsrR, CstR, CtsR, and HrcA regulons. The SACOL2531-29 operon was most strongly upregulated by MHQ and was renamed as mhqRED operon based on its homology to the Bacillus subtilis locus. Here, we characterized the MarR-type regulator MhqR (SACOL2531) as quinone-sensing repressor of the mhqRED operon, which confers quinone and antimicrobial resistance in S. aureus. The mhqRED operon responds specifically to MHQ and less pronounced to pyocyanin and ciprofloxacin, but not to reactive oxygen species (ROS), hypochlorous acid, or aldehydes. The MhqR repressor binds specifically to a 9–9 bp inverted repeat (MhqR operator) upstream of the mhqRED operon and is inactivated by MHQ in vitro, which does not involve a thiol-based mechanism. In phenotypic assays, the mhqR deletion mutant was resistant to MHQ and quinone-like antimicrobial compounds, including pyocyanin, ciprofloxacin, norfloxacin, and rifampicin. In addition, the mhqR mutant was sensitive to sublethal ROS and 24 h post-macrophage infections but acquired an improved survival under lethal ROS stress and after long-term infections. Innovation: Our results provide a link between quinone and antimicrobial resistance via the MhqR regulon of S. aureus. Conclusion: The MhqR regulon was identified as a novel resistance mechanism towards quinone-like antimicrobials and contributes to virulence of S. aureus under long-term infections