28,117 research outputs found

    Phenotypic plasticity in sargassum forests may not counteract projected biomass losses along a broad latitudinal gradient

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    Phenotypic plasticity and local adaptation can adjust individual responses to environmental changes across species' ranges. Studies addressing the implications of such traits have been underrepresented in the marine environment. Sargassum cymosum represents an ideal model to test phenotypic plasticity, as populations along the southwestern Atlantic Ocean display a sharp decrease in abundance toward distributional range limits. We (1) characterized the macroecological environment of S. cymosum across a latitudinal gradient, (2) evaluated potential differences in ecophysiological adjustments (biomass, photosynthetic pigments, phenolic compounds, total soluble sugars and proteins, and carbon-nitrogen-CN-content), and (3) tested for differences in thermal tolerance based on time series analyses produced from the present to contrasting representative concentration pathways scenarios (RCP) of future climate changes. Our results showed distinct macroecological environments, corresponding to tropical and warm temperate conditions, driving biomass and ecophysiological adjustments of S. cymosum. Populations from the two environments displayed contrasting thermal tolerances, with tropical individuals better coping with thermal stress when compared to more temperate ones (lethal temperatures of 33 degrees C vs. 30 degrees C); yet both populations lose biomass in response to increasing thermal stress while increasing secondary metabolites (for example, carotenoids and phenolic compounds) and decrease chlorophyll's content, Fv/Fm, total soluble sugars concentration and CN ratio, owing to oxidative stress. Despite evidence for phenotypic plasticity, significant future losses might occur in both tropical and warm temperate populations, particularly under the no mitigation RCP scenario, also known as the business as usual (that is, 8.5). In this context, broad compliance with the Paris Agreement might counteract projected impacts of climate change, safeguarding Sargassum forests in the years to come.This study was supported by grants from Boticario Foundation, FAPESC-Foundation Support Research and Innovation in the State of Santa Catarina, Capes Higher Education Personnel Improvement Coordination, CNPq-National Council for Scientific and Technological Development, Petrobras Ambiental, REBENTOS-Habitat monitoring network coastal Benthic and ProspecMar-Islands Sustainable Prospecting in Ocean Islands: Biodiversity, Chemistry, Ecology and Biotechnology, Rede Coral Vivo, REDEALGAS, a Pew Marine Fellowship, the Foundation for Science and Technology (FCT) of Portugal via SFRH/BSAB/150485/2019, SFRH/BD/144878/2019, UID/Multi/04326/2019, PTDC/BIA-CBI/6515/2020 and the transitional norm DL57/2016/CP1361/CT0035. LPG received a doctorate scholarship (88882.438723/2019-01) from Capes. CFDG thanks CNPq grants PQ-309658/2016-0and306304/2019-8. PAH thanks CAPES-Senior Visitor, CAPESPrInt 310793/2018-01, CNPq-PVE 407365/2013-3, CNPq-Universal 426215/2016-8 and CNPq-PQ308537/2019-0. GK received a master's scholarship from CAPES.info:eu-repo/semantics/submittedVersio

    Differential responses in some quinoa genotypes of a consortium of beneficial endophytic bacteria against bacterial leaf spot disease

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    Many effective plant-microbe interactions lead to biological changes that can stimulate plant growth and production. This study evaluated the effect of the interaction between quinoa (Chenopodium quinoa Willd.) and endophytic bacterial strains on differential responses under biotic stress. Four strains of endophytic bacteria were used to inoculate three quinoa genotypes. Endophytic bacteria, isolated from the endosphere of healthy genotypes of quinoa plants, were used to evaluate their biocontrol activity against Pseudomonas syringae on quinoa plants, which causes leaf spot disease, depending on some different parameters. Quinoa genotype plants were treated with four treatments: pathogenic bacteria only (T1), internal bacteria only (T2), pathogenic bacteria + endogenous bacteria (T3), and untreated as the control (T4). The results indicated that there was a significant difference between chlorophyll content index of infected plants without bioagent (untreated) compared to plants bio-inoculated with endophytic bacteria. The highest mean disease incidence was on the plants without bacterial inoculum (90, 80, and 100%) for quinoa genotypes G1, G2, and G3, respectively. The results showed that there were significant differences in the weight of grains/plant, as the value ranged from 8.1 to 13.3 g when treated with pathogens (T1) compared to the treatment with pathogens and endogenous bacteria (T3), which ranged from 11.7 to 18.6 g/plant. Decreases in total aromatic amino acids appeared due to the pathogen infection, by 6.3, 22.8, and 24.1% (compared to the control) in G1, G2, and G3, respectively. On the other hand, genotype G3 showed the highest response in the levels of total aromatic and total neutral amino acids. The endophytic strains promoted quinoa seedling growth mainly by improving nutrient efficiency. This improvement could not be explained by their ability to induce the production of amino acids, showing that complex interactions might be associated with enhancement of quinoa seedling performance by endophytic bacteria. The endophytic bacterial strains were able to reduce the severity of bacterial leaf spot disease by 30, 40, and 50% in quinoa genotypes G1, G2, and G3, respectively, recording significant differences compared to the negative control. The results indicated that, G1 genotype was superior in different performance indicators (pathogen tolerance index, yield injury %, superiority measure and relative performance) for grain weight/plant under pathogen infection condition when treated with endophyte bacteria. Based on this study, these bacterial strains can be used as a biotechnology tool in quinoa seedling production and biocontrol to diminish the severity of bacterial leaf spot disease

    Impact of polyester and cotton microfibers on growth and sublethal biomarkers in juvenile mussels

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    Anthropogenic microfibres are a prevalent, persistent and globally distributed form of marine debris. Evidence of microfibre ingestion has been demonstrated in a range of organisms, including Mytilus spp. (mussels), but the extent of any impacts on these organisms are poorly understood. This study investigates, for the first time, the effect of exposing juvenile mussels to polyester and cotton microfibres at environmentally relevant concentrations (both current and predicted future scenarios) over a chronic timescale (94 days). Sublethal biomarkers included growth rate, respiration rate and clearance rate. Mussels were exposed to polyester (median length 149 µm) and cotton (median length 132 µm) microfibres in three treatments: polyester (~ 8 fibres L−1), polyester (~ 80 fibres L−1) and cotton (~ 80 fibres L−1). Mussels exposed to 80 polyester or cotton microfibres L−1 exhibited a decrease in growth rate of 35.6% (polyester) and 18.7% (cotton), with mussels exposed to ~ 80 polyester microfibres L−1 having a significantly lower growth rate than the control population (P < 0.05). This study demonstrates that polyester microfibres have the potential to adversely impact upon mussel growth rates in realistic future scenarios, which may have compounding effects throughout the marine ecosystem and implications for commercial viability

    Biological effects of sub-lethal doses of glyphosate and AMPA on cardiac myoblasts

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    Introduction: Glyphosate is the active compound of different non-selective herbicides, being the most used agriculture pesticide worldwide. Glyphosate and AMPA (one of its main metabolites) are common pollutants of water, soil, and food sources such as crops. They can be detected in biological samples from both exposed workers and general population. Despite glyphosate acts as inhibitor of the shikimate pathway, present only in plants and some microorganisms, its safety in mammals is still debated. Acute glyphosate intoxications are correlated to cardiovascular/neuronal damages, but little is known about the effects of the chronic exposure.Methods: We evaluated the direct biological effects of different concentrations of pure glyphosate/AMPA on a rat-derived cell line of cardiomyoblasts (H9c2) in acute (1–2 h) or sub-chronic (24–48 h) settings. We analyzed cell viability/morphology, ROS production and mitochondrial dynamics.Results: Acute exposure to high doses (above 10 mM) of glyphosate and AMPA triggers immediate cytotoxic effects: reduction in cell viability, increased ROS production, morphological alterations and mitochondrial function. When exposed to lower glyphosate concentrations (1 μM—1 mM), H9c2 cells showed only a slight variation in cell viability and ROS production, while mitochondrial dynamic was unvaried. Moreover, the phenotype was completely restored after 48 h of treatment. Surprisingly, the sub-chronic (48 h) treatment with low concentrations (1 μM—1 mM) of AMPA led to a late cytotoxic response, reflected in a reduction in H9c2 viability.Conclusion: The comprehension of the extent of human exposure to these molecules remains pivotal to have a better critical view of the available data

    A proprietary black cumin oil extract (Nigella sativa) (BlaQmax®) modulates stress-sleep-immunity axis safely: Randomized double-blind placebo-controlled study

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    ObjectiveStress, sleep, and immunity are important interdependent factors that play critical roles in the maintenance of health. It has been established that stress can affect sleep, and the quality and duration of sleep significantly impact immunity. However, single drugs capable of targeting these factors are limited because of their multi-targeting mechanisms. The present study investigated the influence of a proprietary thymoquinone-rich black cumin oil extract (BCO-5) in modulating stress, sleep, and immunity.MethodsA randomized double-blinded placebo-controlled study was carried out on healthy volunteers with self-reported non-refreshing sleep issues (n = 72), followed by supplementation with BCO-5/placebo at 200  mg/day for 90  days. Validated questionnaires, PSQI and PSS, were employed for monitoring sleep and stress respectively, along with the measurement of cortisol and melatonin levels. Immunity markers were analyzed at the end of the study.ResultsIn the BCO-5 group, 70% of the participants reported satisfaction with their sleep pattern on day 7 and 79% on day 14. Additionally, both inter- and intra- group analyses of the total PSQI scores and component scores (sleep latency, duration, efficiency, quality, and daytime dysfunction) on days 45 and 90 showed the effectiveness of BCO-5 in the improvement of sleep (p &lt; 0.05). PSS-14 analysis revealed a significant reduction in stress, upon both intra (p &lt; 0.001) and inter-group (p &lt; 0.001) comparisons. The observed reduction in stress among the BCO-5 group, with respect to the placebo, was significant with an effect size of 1.19 by the end of the study (p &lt; 0.001). A significant correlation was also observed between improved sleep and reduced stress as evident from PSQI and PSS. Furthermore, there was a significant modulation in melatonin, cortisol, and orexin levels. Hematological/immunological parameters further revealed the immunomodulatory effects of BCO-5.ConclusionBCO-5 significantly modulated the stress-sleep-immunity axis with no side effects and restored restful sleep

    Pollution-induced community tolerance in freshwater biofilms – from molecular mechanisms to loss of community functions

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    Exposure to herbicides poses a threat to aquatic biofilms by affecting their community structure, physiology and function. These changes render biofilms to become more tolerant, but on the downside community tolerance has ecologic costs. A concept that addresses induced community tolerance to a pollutant (PICT) was introduced by Blanck and Wängberg (1988). The basic principle of the concept is that microbial communities undergo pollution-induced succession when exposed to a pollutant over a long period of time, which changes communities structurally and functionally and enhancing tolerance to the pollutant exposure. However, the mechanisms of tolerance and the ecologic consequences were hardly studied up to date. This thesis addresses the structural and functional changes in biofilm communities and applies modern molecular methods to unravel molecular tolerance mechanisms. Two different freshwater biofilm communities were cultivated for a period of five weeks, with one of the communities being contaminated with 4 μg L-1 diuron. Subsequently, the communities were characterized for structural and functional differences, especially focusing on their crucial role of photosynthesis. The community structure of the autotrophs was assessed using HPLC-based pigment analysis and their functional alterations were investigated using Imaging-PAM fluorometry to study photosynthesis and community oxygen profiling to determine net primary production. Then, the molecular fingerprints of the communities were measured with meta-transcriptomics (RNA-Seq) and GC-based community metabolomics approaches and analyzed with respect to changes in their molecular functions. The communities were acute exposed to diuron for one hour in a dose-response design, to reveal a potential PICT and uncover related adaptation to diuron exposure. The combination of apical and molecular methods in a dose-response design enabled the linkage of functional effects of diuron exposure and underlying molecular mechanisms based on a sensitivity analysis. Chronic exposure to diuron impaired freshwater biofilms in their biomass accrual. The contaminated communities particularly lost autotrophic biomass, reflected by the decrease in specific chlorophyll a content. This loss was associated with a change in the molecular fingerprint of the communities, which substantiates structural and physiological changes. The decline in autotrophic biomass could be due to a primary loss of sensitive autotrophic organisms caused by the selection of better adapted species in the course of chronic exposure. Related to this hypothesis, an increase in diuron tolerance has been detected in the contaminated communities and molecular mechanisms facilitating tolerance have been found. It was shown that genes of the photosystem, reductive-pentose phosphate cycle and arginine metabolism were differentially expressed among the communities and that an increased amount of potential antioxidant degradation products was found in the contaminated communities. This led to the hypothesis that contaminated communities may have adapted to oxidative stress, making them less sensitive to diuron exposure. Moreover, the photosynthetic light harvesting complex was altered and the photoprotective xanthophyll cycle was increased in the contaminated communities. Despite these adaptation strategies, the loss of autotrophic biomass has been shown to impair primary production. This impairment persisted even under repeated short-term exposure, so that the tolerance mechanisms cannot safeguard primary production as a key function in aquatic systems.:1. The effect of chemicals on organisms and their functions .............................. 1 1.1 Welcome to the anthropocene .......................................................................... 1 1.2 From cellular stress responses to ecosystem resilience ................................... 3 1.2.1 The individual pursuit for homeostasis ....................................................... 3 1.2.2 Stability from diversity ................................................................................. 5 1.3 Community ecotoxicology - a step forward in monitoring the effects of chemical pollution? ................................................................................................................. 6 1.4 Functional ecotoxicological assessment of microbial communities ................... 9 1.5 Molecular tools – the key to a mechanistic understanding of stressor effects from a functional perspective in microbial communities? ...................................... 12 2. Aims and Hypothesis ......................................................................................... 14 2.1 Research question .......................................................................................... 14 2.2 Hypothesis and outline .................................................................................... 15 2.3 Experimental approach & concept .................................................................. 16 2.3.1 Aquatic freshwater biofilms as model community ..................................... 16 2.3.2 Diuron as model herbicide ........................................................................ 17 2.3.3 Experimental design ................................................................................. 18 3. Structural and physiological changes in microbial communities after chronic exposure - PICT and altered functional capacity ................................................. 21 3.1 Introduction ..................................................................................................... 21 3.2 Methods .......................................................................................................... 23 3.2.1 Biofilm cultivation ...................................................................................... 23 3.2.2 Dry weight and autotrophic index ............................................................. 23 3.2.4 Pigment analysis of periphyton ................................................................. 23 3.2.4.1 In-vivo pigment analysis for community characterization ....................... 24 3.2.4.2 In-vivo pigment analysis based on Imaging-PAM fluorometry ............... 24 3.2.4.3 In-vivo pigment fluorescence for tolerance detection ............................. 26 3.2.4.4 Ex-vivo pigment analysis by high-pressure liquid-chromatography ....... 27 3.2.5 Community oxygen metabolism measurements ....................................... 28 3.3 Results and discussion ................................................................................... 29 3.3.1 Comparison of the structural community parameters ............................... 29 3.3.2 Photosynthetic activity and primary production of the communities after selection phase ................................................................................................. 33 3.3.3 Acquisition of photosynthetic tolerance .................................................... 34 3.3.4 Primary production at exposure conditions ............................................... 36 3.3.5 Tolerance detection in primary production ................................................ 37 3.4 Summary and Conclusion ........................................................................... 40 4. Community gene expression analysis by meta-transcriptomics ................... 41 4.1 Introduction to meta-transcriptomics ............................................................... 41 4.2. Methods ......................................................................................................... 43 4.2.1 Sampling and RNA extraction................................................................... 43 4.2.2 RNA sequencing analysis ......................................................................... 44 4.2.3 Data assembly and processing................................................................. 45 4.2.4 Prioritization of contigs and annotation ..................................................... 47 4.2.5 Sensitivity analysis of biological processes .............................................. 48 4.3 Results and discussion ................................................................................... 48 4.3.1 Characterization of the meta-transcriptomic fingerprints .......................... 49 4.3.2 Insights into community stress response mechanisms using trend analysis (DRomic’s) ......................................................................................................... 51 4.3.3 Response pattern in the isoform PS genes .............................................. 63 4.5 Summary and conclusion ................................................................................ 65 5. Community metabolome analysis ..................................................................... 66 5.1 Introduction to community metabolomics ........................................................ 66 5.2 Methods .......................................................................................................... 68 5.2.1 Sampling, metabolite extraction and derivatisation................................... 68 5.2.2 GC-TOF-MS analysis ............................................................................... 69 5.2.3 Data processing and statistical analysis ................................................... 69 5.3 Results and discussion ................................................................................... 70 5.3.1 Characterization of the metabolic fingerprints .......................................... 70 5.3.2 Difference in the metabolic fingerprints .................................................... 71 5.3.3 Differential metabolic responses of the communities to short-term exposure of diuron ............................................................................................................ 73 5.4 Summary and conclusion ................................................................................ 78 6. Synthesis ............................................................................................................. 79 6.1 Approaches and challenges for linking molecular data to functional measurements ...................................................................................................... 79 6.2 Methods .......................................................................................................... 83 6.2.1 Summary on the data ............................................................................... 83 6.2.2 Aggregation of molecular data to index values (TELI and MELI) .............. 83 6.2.3 Functional annotation of contigs and metabolites using KEGG ................ 83 6.3 Results and discussion ................................................................................... 85 6.3.1 Results of aggregation techniques ........................................................... 85 6.3.2 Sensitivity analysis of the different molecular approaches and endpoints 86 6.3.3 Mechanistic view of the molecular stress responses based on KEGG functions ............................................................................................................ 89 6.4 Consolidation of the results – holistic interpretation and discussion ............... 93 6.4.1 Adaptation to chronic diuron exposure - from molecular changes to community effects.............................................................................................. 93 6.4.2 Assessment of the ecological costs of Pollution-induced community tolerance based on primary production ............................................................. 94 6.5 Outlook ............................................................................................................ 9

    Long-term strenuous exercise promotes vascular injury by selectively damaging the tunica media: experimental evidence

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    Moderate exercise has well-founded benefits in cardiovascular health. However, increasing, yet controversial, evidence suggests that extremely trained athletes may not be protected from cardiovascular events as much as moderately trained individuals. In our rodent model, intensive but not moderate training promoted aorta and carotid stiffening and elastic lamina ruptures, tunica media thickening of intramyocardial arteries, and an imbalance between vasoconstrictor and relaxation agents. An up-regulation of angiotensin-converter enzyme, miR-212, miR-132, and miR-146b might account for this deleterious remodeling. Most changes remained after a 4-week detraining. In conclusion, our results suggest that intensive training blunts the benefits of moderate exercise

    Bioaccumulation of CuO nanomaterials in rainbow trout: influence of exposure route and particle shape

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    The bioaccumulation potential of spherical and rod-shaped CuO nanomaterials (NMs) was assessed in rainbow trout (Oncorhynchus mykiss) exposed via water and diet following the OECD Test Guideline No. 305. Fish were exposed via diet to both NMs at concentrations of 70 and 500 mg Cu/kg for 15 days, followed by 44 days of depuration. For water-borne exposure, only the rod-shaped CuO NMs were tested at 0.08 and 0.8 mg Cu/L for 28 days, followed by 14 days of depuration. The concentration of Cu was determined in fish whole body to derive biomagnification and bioconcentration factors (BMF and BCF). Different tissues were sampled to investigate the total Cu biodistribution and target organs as well as the particle number-based bioaccumulation of CuO NMs. Estimated BMF and BCF values were below the thresholds of concern. However, shape and route influenced depuration. Following dietary exposure, there was a higher depuration of Cu from fish exposed to the rod-shaped compared to the spherical CuO NMs. A higher depuration was also observed for rod-shaped CuO NMs following the dietary exposure compared the aqueous one. Despite the much higher dietary exposure concentrations of rod-shape CuO NMs, similar Cu body burdens were reached via water. Cu was found in particulate form in different tissues.Although these NMs had a low bioaccumulation potential, differences in distribution and elimination patterns of Cu were observed depending on the exposure route and particle shape. Careful consideration of the most relevant exposure route is needed when designing a bioaccumulation experiment for testing NMs.Environmental Biolog

    Alterations to cerebral perfusion, metabolite profiles, and neuronal morphology in the hippocampus and cortex of male and female mice during chronic exposure to a high-salt diet

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    Excess dietary salt reduces resting cerebral blood flow (CBF) and vascular reactivity, which can limit the fueling of neuronal metabolism. It is hitherto unknown whether metabolic derangements induced by high-salt-diet (HSD) exposure during adulthood are reversed by reducing salt intake. In this study, male and female mice were fed an HSD from 9 to 16 months of age, followed by a normal-salt diet (ND) thereafter until 23 months of age. Controls were continuously fed either ND or HSD. CBF and metabolite profiles were determined longitudinally by arterial spin labeling magnetic resonance imaging and magnetic resonance spectroscopy, respectively. HSD reduced cortical and hippocampal CBF, which recovered after dietary salt normalization, and affected hippocampal but not cortical metabolite profiles. Compared to ND, HSD increased hippocampal glutamine and phosphocreatine levels and decreased creatine and choline levels. Dietary reversal only allowed recovery of glutamine levels. Histology analyses revealed that HSD reduced the dendritic arborization and spine density of cortical and hippocampal neurons, which were not recovered after dietary salt normalization. We conclude that sustained HSD exposure throughout adulthood causes permanent structural and metabolic alterations to the mouse brain that are not fully normalized by lowering dietary salt during aging

    Selenium nanoparticles modulate histone methylation via lysine methyltransferase activity and S-adenosylhomocysteine depletion

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    At physiological levels, the trace element selenium plays a key role in redox reactions through the incorporation of selenocysteine in antioxidant enzymes. Selenium has also been evaluated as a potential anti-cancer agent, where selenium nanoparticles have proven effective, and are well tolerated in vivo at doses that are toxic as soluble Se. The use of such nanoparticles, coated with either serum albumin or the naturally occurring alkaline polysaccharide chitosan, also serves to enhance biocompatibility and bioavailability. Here we demonstrate a novel role for selenium in regulating histone methylation in ovarian cancer cell models treated with inorganic selenium nanoparticles coated with serum albumin or chitosan. As well as inducing thioredoxin reductase expression, ROS activity and cancer cell cytotoxicity, coated nanoparticles caused significant increases in histone methylation. Specifically, selenium nanoparticles triggered an increase in the methylation of histone 3 at lysines K9 and K27, histone marks involved in both the activation and repression of gene expression, thus suggesting a fundamental role for selenium in these epigenetic processes. This direct function was confirmed using chemical inhibitors of the histone lysine methyltransferases EZH2 (H3K27) and G9a/EHMT2 (H3K9), both of which blocked the effect of selenium on histone methylation. This novel role for selenium supports a distinct function in histone methylation that occurs due to a decrease in S-adenosylhomocysteine, an endogenous inhibitor of lysine methyltransferases, the metabolic product of methyl-group transfer from S-adenosylmethionine in the one-carbon metabolism pathway. These observations provide important new insights into the action of selenium nanoparticles. It is now important to consider both the classic antioxidant and novel histone methylation effects of this key redox element in its development in cancer therapy and other applications
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