scholarly journals Disparate effects of antibiotic-induced microbiome change and enhanced fitness inDaphnia magna

2019 ◽  
Author(s):  
Asa Motiei ◽  
Björn Brindefalk ◽  
Martin Ogonowski ◽  
Rehab El-Shehawy ◽  
Paulina Pastuszek ◽  
...  
Keyword(s):  
Antioxidant Capacity ◽  
Diversity Indices ◽  
Supporting Evidence ◽  
Dependent Manner ◽  
Antibiotic Exposure ◽  
Concentration Dependent Manner ◽  
Common View ◽  
Host Fitness ◽  
Mediated Effects ◽  
Early Effects

AbstractIt is a common view that an organism’s microbiota has a profound influence on host fitness; however, supporting evidence is lacking in many organisms. We manipulated the gut microbiome ofDaphnia magnaby chronic exposure to different concentrations of the antibiotic Ciprofloxacin (0.01 – 1 mg L−1), and evaluated whether this affected the animals’ fitness and antioxidant capacity. In line with our expectations, antibiotic exposure altered the microbiome in a concentration-dependent manner. However, contrary to these expectations, the reduced diversity of gut bacteria was not associated with any fitness detriment. Moreover, the growth-related parameters correlated negatively with diversity indices; and, in the daphnids exposed to the lowest ciprofloxacin concentrations, the antioxidant capacity, growth, and fecundity were even higher than in control animals. These findings suggest that ciprofloxacin exerts direct stimulatory effects on growth and reproduction inDaphnia, while microbiome-mediated effects are of lesser importance. Thus, although microbiome profiling of Daphnia may be a sensitive tool to identify early effects of antibiotic exposure, disentangling direct and microbiome-mediated effects on host fitness is not straightforward.

scholarly journals Assessment of Chitosan-Rue (Ruta graveolens L.) Essential Oil-Based Coatings on Refrigerated Cape Gooseberry (Physalis peruviana L.) Quality

2020 ◽  
Vol 10 (8) ◽  
pp. 2684
Author(s):  
María González-Locarno ◽  
Yarley Maza Pautt ◽  
Alberto Albis ◽  
Edwin Florez López ◽  
Carlos David Grande Tovar
Keyword(s):  
Essential Oil ◽  
Antioxidant Capacity ◽  
Lower Amount ◽  
Edible Coatings ◽  
Dependent Manner ◽  
Ruta Graveolens ◽  
Concentration Dependent Manner ◽  
Physalis Peruviana ◽  
Dpph Method ◽  
Cape Gooseberry

Cape gooseberry (Physalis peruviana L.) is one of the main exotic fruits in demand throughout the world market. However, this fruit has problems with physical and microbial decay causing losses up to thirty percent during post-harvest stage and market storage. As an alternative for conservation, technologies based on edible coatings of biopolymers incorporating essential oils have been developed. In this paper we studied the effect of edible coatings based on chitosan (CS) and Ruta graveolens L. essential oil (RGEO) at different concentrations applied on the surface gooseberries at 18 ± 2 °C. The emulsions exhibited a reduction in the viscosity and the particle size with the increasing in the RGEO amount (from 124.7 cP to 26.0 cP for CS + RGEO 0.5% and CS + RGEO 1.5%, respectively). A lower weight loss was obtained for fruits coated with CS + RGEO 0.5% (12.7%) as compared to the uncoated (15%), while the maturity index increased in a lower amount for CS + RGEO coated than the uncoated fruits. The mesophyll growth was delayed three days after the coating applications for CS + RGEO 1.0% and 1.5%. At day twelve of the coating process, fruits with CS + RGEO 1.5% presented only 3.1 Log UFC/g of aerobic mesophylls and 2.9 Log UFC/g of molds and yeasts, while the uncoated fruits presented 4.2 Log UFC/g of aerobic mesophylls and 4.0 Log UFC/g of molds and yeasts, demonstrating a microbial barrier of the coatings incorporating RGEO in a concentration dependent manner. The CS + RGEO coating also preserve the antioxidant property of case gooseberries after twelve days of treatment under storage according to the 2,2′-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2′-azinobis-(3-ethyl-benzothiazoline-6-sulphonic acid) (ABTS) results. It was demonstrated by the ABTS method that T5 antioxidant capacity from day one to day twelve only decreases from 55% to 44%, while in the uncoated fruits (T1) the antioxidant capacity decreased from 65% to 18%. On the other hand, using the DPPH method the reduction was from 73% to 24% for the uncoated samples and 55% to 43% for T5. From the sensorial analysis, we recommend the use of CS + RGEO 0.5% that was still accepted by the panelists after the sixth day of application. These results show the potential application of these coatings as postharvest treatment under storage and low temperature conditions during twelve days of treatment for cape gooseberry fruits.

scholarly journals Use of Parabens (Methyl and Butyl) during the Gestation Period: Mitochondrial Bioenergetics of the Testes and Antioxidant Capacity Alterations in Testes and Other Vital Organs of the F1 Generation

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1302
Author(s):  
Maria Manuel Oliveira ◽  
Fátima Martins ◽  
Mónica G. Silva ◽  
Elisete Correia ◽  
Romeu Videira ◽  
...  
Keyword(s):  
Antioxidant Capacity ◽  
Germ Cells ◽  
Citrate Synthase ◽  
Respiratory Control ◽  
Mitochondrial Bioenergetics ◽  
Dependent Manner ◽  
Glutathione S Transferase ◽  
Concentration Dependent Manner ◽  
Female Wistar Rats ◽  
F1 Generation

Since the mid-1920s, parabens have been widely used as antimicrobial preservatives in processed foods and beverages, pharmaceuticals, and cosmetic products. Paraben use continues to generate considerable controversy, both in the general population and in the scientific community itself. The primary purpose of our study was to determine whether parabens (methyl and butyl at concentrations of 100 and 200 mg/kg body weight by subcutaneous injection) during pregnancy of adult female Wistar rats can have an impact on the F1 generation. As far as we know, we are the first to demonstrate that using parabens during pregnancy has negative repercussions on the mitochondrial bioenergetics and antioxidant activity of testicular germ cells in the F1 generation. Our study showed that there was a 48.7 and 59.8% decrease in the respiratory control index with 100 and 200 mg/kg of butylparaben, respectively. Cytochrome c oxidase activity was significantly inhibited (45 and 51%) in both groups. In addition, 200 mg/kg butylparaben promoted a marked decrease in citrate synthase activity, indicating that mitochondrial content decreased in the germ cells, especially spermatocytes and spermatids. Mitochondrial ROS production increased in groups exposed to parabens in a concentration-dependent manner, especially the butyl one (102 and 130%). The groups exposed to butylparaben showed an increase in superoxide dismutase (SOD) and catalase (CAT) activities, while glutathione reductase (GR) and glutathione S-transferase (GST) decreased. With methylparaben, only differences in SOD and GR were observed; for the latter, this only occurred with the highest concentration. The glutathione (GSH)/glutathione disulfide (GSSG) ratio did not undergo any significant change. However, there was a considerable increase in hydroperoxide content in animals exposed to butylparaben, with 100 and 200 mg/kg resulting in 98.6 and 188% increase, respectively. Furthermore, several other organs also showed alterations in antioxidant capacity due to paraben use. In summary, our study demonstrates that paraben use during pregnancy will cause severe changes in the mitochondrial bioenergetics and antioxidant capacity of testicular germ cells and the antioxidant capacity of several other F1 generation organs.

scholarly journals Chemopreventive Effects and Antioxidant Capacity of Combined Leaf Extracts of Sesamum angustifolium (Oliv.) Engl. and Hibiscus articulatus on Rhabdomyosarcoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Clayton E. Siamayuwa ◽  
Loveness K. Nyanga ◽  
Cathrine Chidewe
Keyword(s):  
Antioxidant Capacity ◽  
Cell Line ◽  
Caspase 3 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Leaf Extracts ◽  
Concentration Dependent Manner ◽  
Rd Cells ◽  
Antioxidant Capacity Assays ◽  
Increased Activity

Sesamum angustifolium (Oliv.) Engl. and Hibiscus articulatus contain compounds that have antimutagenic properties. The rise in rhabdomyosarcoma in paediatrics and prognosis of the disease in infants compared to adults calls for newer, less toxic alternatives in treatment of the disease. The aim of this study was to determine the anticancer activity and antioxidant capacity of combined leaf extracts of Sesamum angustifolium (Oliv.) Engl. and Hibiscus articulatus (SAHA), against rhabdomyosarcoma (RMS) using rhabdomyosarcoma (RD) cell line and mouse (L20B) cell line. Cytotoxicity, morphology, apoptosis induction, and antioxidant capacity assays were done. Of the four solvents used for extraction, the dichloromethane SAHA extract was the most cytotoxic with IC50 of 106 μg/mL after doxorubicin, the reference anticancer drug with IC50 of 0.8 μg/mL. The SAHA extracts had a stronger cytotoxicity effect on the cancerous RD cells than on normal L20B cells. Morphological assessment showed untreated cells maintained their normal striated appearance of muscle cells whereas cells treated with doxorubicin or SAHA extracts exhibited cell shrinkage, loss of surface adherence, reduced cell density along with cell debris, which is a characteristic of apoptosis. Normal L20B cells when treated with doxorubicin or SAHA extracts, maintained their cell shape, and remained adherent to the surface. The apoptotic enzyme caspase-3 was induced in a concentration dependent manner upon treatment of the RD cells with SAHA extracts or doxorubicin. Induction of caspase-3 was ten times less in treated L20B cells compared to the RD cells. Low induction of caspase-9 enzyme was observed in both treated RD and L20B cells. Treatment of both RD and L20B cells with SAHA extracts or doxorubicin resulted in increased activity of peroxidase and reduction of oxidative stress. Results of the study show that the SAHA extracts are potential sources of compounds that may serve as useful agents for treatment of rhabdomyosarcoma.

Mitochondrial localization of ERα and ERβ in human MCF7 cells

2004 ◽  
Vol 286 (6) ◽  
pp. E1011-E1022 ◽  
Author(s):  
Jin Q. Chen ◽  
Michael Delannoy ◽  
Carol Cooke ◽  
James D. Yager
Keyword(s):  
Rat Hepatocytes ◽  
Mitochondrial Respiratory Chain ◽  
Immunogold Electron Microscopy ◽  
Dependent Manner ◽  
Mcf7 Cells ◽  
Concentration Dependent Manner ◽  
Transcript Levels ◽  
Mediated Effects ◽  
Targeting Peptide ◽  
Additional Support

We observed previously that estrogen treatment increased the transcript levels of several mitochondrial DNA (mtDNA)-encoded genes for mitochondrial respiratory chain (MRC) proteins and MRC activity in rat hepatocytes and human Hep G2 cells. Others have reported detection of estrogen receptors (ER), ERα and ERβ, in mitochondria of rabbit ovarian and uterine tissue. In this study, we have extended these observations. Using cellular fractionation and Western blot with ERα- and ERβ-specific antibodies, we observed that ERα and ERβ are present in mitochondria of human MCF7 cells and that the mitochondrial ERα and ERβ account for 10 and 18%, respectively, of total cellular ERα and ERβ in 17β-estradiol (E2)-treated MCF7 cells. We also found that E2 significantly enhanced the amounts of mitochondrial ERα and ERβ in a time- and concentration-dependent manner and that these effects are accompanied by a significant increase in the transcript levels of mtDNA-encoded genes, i.e., cytochrome c oxidase subunits I and II. Moreover, we demonstrated that these E2-mediated effects were inhibited by the pure ER antagonist, ICI-182780, indicating the involvement of ERs. Using immunohistochemistry with confocal microscopy and immunogold electron microscopy, we demonstrated that ERα and ERβ are located within the MCF7 cell mitochondrial matrix. Computer analysis identified a putative internal mitochondrial targeting peptide signal within human ERβ, suggesting an inherent potential for ERβ to enter mitochondria. These findings confirm the observations of others and provide additional support for this novel localization of the ERs and for a potentially important role of the ER in the regulation of mtDNA transcription.

Midazolam Selectively Potentiates the A2A- but not A1-receptor– mediated Effects of Adenosine

2000 ◽  
Vol 92 (2) ◽  
pp. 567-567 ◽  
Author(s):  
Christoph N. Seubert ◽  
Timothy E. Morey ◽  
Anatoly E. Martynyuk ◽  
Roy F. Cucchiara ◽  
Donn M. Dennis
Keyword(s):  
Guinea Pig ◽  
Dependent Manner ◽  
Nucleoside Transporter ◽  
Binding Assays ◽  
A2a Adenosine Receptor ◽  
Concentration Dependent Manner ◽  
Isolated Hearts ◽  
Mediated Effects ◽  
Competition Binding ◽  
A1 Receptor

Background Inhibition of adenosine metabolism offers a unique approach to harness the cardioprotective properties of adenosine in a site- and event-specific manner. Benzodiazepines inhibit adenosine metabolism by blocking nucleoside transporter. Therefore, the authors studied the binding affinities of structurally different benzodiazepines to nucleoside transporter and benzodiazepine-induced potentiation of A1-adenosine (negative dromotropy) and A2A-adenosine (coronary vasodilation) receptor-mediated effects. Methods In membranes from porcine striatum and guinea pig ventricle, competition binding assays to displace [3H]nitrobenzylmercaptopurine riboside ([3H]NBMPR) from nucleoside transporter were performed using alprazolam, chlorodiazepoxide, diazepam, flurazepam, and midazolam. The augmentation by the most potent benzodiazepine of A1- and A2A-adenosine receptor-mediated responses, elicited by exogenous administration of adenosine or brief periods of global hypoxia, was subsequently studied in guinea pig Langendorff-perfused hearts. Results All benzodiazepines completely displaced [3H]NBMPR in a concentration-dependent manner with Hill coefficients not significantly different from unity in both striatal and ventricular membranes. Midazolam was the most potent inhibitor of nucleoside transporter (ventricle:pKi = 5.22+/-0.41, Ki = 6 microM). In isolated hearts, midazolam (5, 10, 20 microM) significantly augmented coronary flow in a concentration-dependent manner in the presence of adenosine (30 nM), an effect reversed by ZM 241385, a selective A2A-receptor antagonist. In contrast, midazolam did not increase the effect of adenosine (30 nM) on atrioventricular conduction. Similarly, midazolam potentiated A2A- but not A1-receptor-mediated effects of endogenous adenosine released during hypoxia. Conclusions Structurally distinct benzodiazepines inhibit nucleoside transporter to different degrees. Midazolam selectively augments A2A- but not A1-receptor-mediated effects of adenosine by inhibiting nucleoside transporter.

The Anti-Atherogenic Properties of Sesamin are Mediated via Improved Macrophage Cholesterol Efflux Through PPARγ1-LXRα and MAPK Signaling

2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro
Keyword(s):  
Cholesterol Efflux ◽  
Transcriptional Activity ◽  
Molecular Mechanisms ◽  
Foam Cell ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Foam Cell Formation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Macrophage Cholesterol Efflux

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.

Neutrophil Elastase Potentiates Cathepsin G-lnduced Platelet Activation

1992 ◽  
Vol 68 (05) ◽  
pp. 570-576 ◽  
Author(s):  
Mary A Selak
Keyword(s):  
Neutrophil Elastase ◽  
Cell Activation ◽  
Thromboxane A2 ◽  
Creatine Phosphate ◽  
Dense Granule ◽  
Cathepsin G ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Low Concentrations ◽  
High Concentrations

SummaryWe have previously demonstrated that human neutrophil cathepsin G is a strong platelet agonist that binds to a specific receptor. This work describes the effect of neutrophil elastase on cathepsin G-induced platelet responses. While platelets were not activated by high concentrations of neutrophil elastase by itself, elastase enhanced aggregation, secretion and calcium mobilization induced by low concentrations of cathepsin G. Platelet aggregation and secretion were potentiated in a concentration-dependent manner by neutrophil elastase with maximal responses observable at 200 nM. Enhancement was observed when elastase was preincubated with platelets for time intervals of 10–60 s prior to addition of a low concentration of cathepsin G and required catalytically-active elastase since phenylmethanesulphonyl fluoride-inhibited enzyme failed to potentiate cell activation. Neutrophil elastase potentiation of platelet responses induced by low concentrations of cathepsin G was markedly inhibited by creatine phosphate/creatine phosphokinase and/or indomethacin, indicating that the synergism between elastase and cathepsin G required the participation of ADP and thromboxane A2. On the other hand, platelet responses were not attenuated by the PAF antagonist BN 52021, signifying that PAF-acether did not play a role in elastase potentiation. At higher concentrations porcine pancreatic elastase exhibits similar effects to neutrophil elastase, demonstrating that the effect of elastase was not unique to the neutrophil protease. While neutrophil elastase failed to alter the ability of cathepsin G to hydrolyze a synthetic chromogenic substrate, preincubation of platelets with elastase increased the apparent affinity of cathepsin G binding to platelets. In contrast to their effect on cathepsin G-induced platelet responses, neither neutrophil nor pancreatic elasatse potentiated aggregation or dense granule release initiated by ADP, PAF-acether, arachidonic acid or U46619, a thromboxane A2 mimetic. Moreover, unlike its effect on cathepsin G, neutrophil elastase inhibited thrombin-induced responses. The current observations demonstrate that elastase can potentiate platelet responses mediated by low concentrations of cathepsin G, suggesting that both enzymes may function synergistically to activate platelets under conditions where neutrophil degranulation occurs.

Trimucytin: A Collagen-Like Aggregating Inducer Isolated from Trimeresurus mucrosquamatus Snake Venom

1993 ◽  
Vol 69 (03) ◽  
pp. 286-292 ◽  
Author(s):  
Che-Ming Teng ◽  
Feng-Nien Ko ◽  
Inn-Ho Tsai ◽  
Man-Ling Hung ◽  
Tur-Fu Huang
Keyword(s):  
Platelet Aggregation ◽  
Snake Venom ◽  
Inositol Phosphate ◽  
Shape Change ◽  
Platelet Activating Factor ◽  
Atp Release ◽  
Platelet Membrane ◽  
Thromboxane B2 ◽  
Dependent Manner ◽  
Concentration Dependent Manner

SummaryTrimucytin is a potent platelet aggregation inducer isolated from Trimeresurus mucrosquamatus snake venom. Similar to collagen, trimucytin has a run of (Gly-Pro-X) repeats at the N-terminal amino acids sequence. It induced platelet aggregation, ATP release and thromboxane formation in rabbit platelets in a concentration-dependent manner. The aggregation was not due to released ADP since it was not suppressed by creatine phosphate/creatine phosphokinase. It was not either due to thromboxane A2 formation because indomethacin and BW755C did not have any effect on the aggregation even thromboxane B2 formation was completely abolished by indomethacin. Platelet-activating factor (PAF) was not involved in the aggregation since a PAF antagonist, kadsurenone, did not affect. However, RGD-containing peptide triflavin inhibited the aggregation, but not the release of ATP, of platelets induced by trimucytin. Indomethacin, mepacrine, prostaglandin E1 and tetracaine inhibited the thromboxane B2 formation of platelets caused by collagen and trimucytin. Forskolin and sodium nitroprusside inhibited both platelet aggregation and ATP release, but not the shape change induced by trimucytin. In quin-2 loaded platelets, the rise of intracellular calcium concentration caused by trimucytin was decreased by 12-O-tetradecanoyl phorbol-13 acetate, imipramine, TMB-8 and indomethacin. In the absence of extracellular calcium, both collagen and trimucytin caused no thromboxane B2 formation, but still induced ATP release which was completely blocked by R 59022. Inositol phosphate formation in platelets was markedly enhanced by trimucytin and collagen. MAB1988, an antibody against platelet membrane glycoprotein Ia, inhibited trimucytinand collagen-induced platelet aggregation and ATP release. However, trimucytin did not replace the binding of 125I-labeled MAB1988 to platelets. Platelets pre-exposed to trimucytin were resistant to the second challenge with trimucytin itself or collagen. It is concluded that trimucytin may activate collagen receptors on platelet membrane, and cause aggregation and release mainly through phospholipase C-phosphoinositide pathway.

Influence of Brain Gangliosides on the Formation and Properties of Supported Lipid Bilayers for Binding Kinetics Studies

2018 ◽  
Author(s):  
Luke Jordan ◽  
Nathan Wittenberg
Keyword(s):  
Lipid Bilayers ◽  
Binding Kinetics ◽  
Supported Lipid Bilayers ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Supported Lipid Bilayer ◽  
Head Groups ◽  
Lipid Diffusion ◽  
Kinetics Of ◽  
Brain Gangliosides

This is a comprehensive study of the effects of the four major brain gangliosides (GM1, GD1b, GD1a, and GT1b) on the adsorption and rupture of phospholipid vesicles on SiO2 surfaces for the formation of supported lipid bilayer (SLB) membranes. Using quartz crystal microbalance with dissipation monitoring (QCM-D) we show that gangliosides GD1a and GT1b significantly slow the SLB formation process, whereas GM1 and GD1b have smaller effects. This is likely due to the net ganglioside charge as well as the positions of acidic sugar groups on ganglioside glycan head groups. Data is included that shows calcium can accelerate the formation of ganglioside-rich SLBs. Using fluorescence recovery after photobleaching (FRAP) we also show that the presence of gangliosides significantly reduces lipid diffusion coefficients in SLBs in a concentration-dependent manner. Finally, using QCM-D and GD1a-rich SLB membranes we measure the binding kinetics of an anti-GD1a antibody that has similarities to a monoclonal antibody that is a hallmark of a variant of Guillain-Barre syndrome.

Sign in / Sign up

Export Citation Format

Share Document