High-throughput screening and molecular dynamics simulations of natural products targeting LuxS/AI-2 system as a novel antibacterial strategy for antibiotic resistance in Helicobacter pylori.

The main goal of treating any Helicobacter pylori (H. pylori)-related gastrointestinal disease is completely eradicating infection. Falling eradication efficiency, off-target effects, and patient noncompliance with prolonged and broad spectrums have sparked clinical interest in exploring other effective, safer therapeutic choices. As natural substances are risk-free and privileged with high levels of antibacterial activity, most of these natural chemical's specific modes of action are unknown. With the aid of in silico molecular docking-based virtual screening studies and molecular dynamic simulations, the current study is intended to gather data on numerous such natural chemicals and assess their affinity for the S-ribosyl homocysteine lyase (LuxS) protein of H. pylori. The ligand with the highest binding energy with LuxS, glucoraphanin, catechin gallate and epigallocatechin gallate were rationally selected for further computational analysis. The solution stability of the three compounds' optimal docking postures with LuxS was initially assessed using long-run molecular dynamics simulations. Using molecular dynamics simulation, the epigallocatechin gallate was found to be the most stable molecule with the highest binding free energy, indicating that it might compete with the natural ligand of the inhibitors. According to ADMET analysis, his phytochemical was a promising therapeutic candidate for an antibacterial action since it had a range of physicochemical, pharmacokinetic, and drug-like qualities and had no discernible adverse effects. Additional in vitro, in vivo, and clinical trials are needed to confirm the drug's precise efficacy during H. pylori infection.Communicated by Ramaswamy H. Sarma.

Coconut coir-derived nanocellulose as an efficient adsorbent for removal of cationic dye safranin-O: a detailed mechanistic adsorption study.

Coconut (Cocos nucifera) coir is an abundant agricultural waste prevalent worldwide. Utilization of this waste has been carried out in this study by obtaining nanocellulose (NC) fibres for wastewater remediation purposes. Nanocellulose was obtained from coconut coir using bleaching and acid-alkali treatments followed by ultrasonication and lyophilization. The structural, compositional, surface and thermal properties of the synthesized material were identified using transmission electron microscopy (TEM), scanning electron microscopy (SEM), powder X-ray diffraction (PXRD), Fourier transform infrared spectroscopy (FT-IR), N2 adsorption/desorption, differential thermal (DT) and derivative thermogravimetric (DTG) analyses. These analyses confirmed the synthesized NC with enhanced thermal stability and porosity which was further used for adsorption process. After synthesis, NC was used for the removal of cationic dye safranin-O from water under ambient conditions through batch adsorption studies. The batch adsorption studies revealed that at 10 ppm of dye concentration, above 99% removal was achieved by 100 mg dosage of NC within 4.5 h at room temperature with qe (maximum adsorption capacity at equilibrium) value of around 83 mg g-1. The corresponding adsorption process fitted well with Langmuir isotherm and pseudo-second order kinetics. The primary mode of adsorption from the thermodynamic studies was found to be chemisorption. The adsorption process was achieved through response surface methodology (RSM) study which revealed that at optimized conditions of temperature 35 °C with a dose of 137.50 mg and contact time of 180 min, above 99% of dye (conc. 0.01 mg mL-1) was removed. In addition, the adsorbent can be recycled up to six cycles without any significant loss of its adsorption capacity. The present comprehensive study revealed that a greener eco-friendly synthesis of NC from waste material coconut coir was an effective nanoadsorbent for dye removal with high efficacy. This surely opens up opportunities to develop sustainable protocols for efficient environmental remediation.

Fluoranthene-terminated terpyridine ensemble for fluorescence light up and ratiometric chemical sensor for multi toxic metals.

A novel π-electron rich fluoranthene embellished with a phenyl spacer and coupled with terpyridine (TS1) was developed through Diels-Alder reaction. Single crystal X-ray structure evidences the variations in dihedral angles between the fluoranthene and the phenyl unit responsible for development of non-coplanar interactions and stabilized by a wave-like molecular packing in the crystal lattice with weak π-π interaction of 4.125 Å. The peripheral terpyridine of TS1 endows an efficient binding with multiple metal ions by colorimetric and fluorometric methods. TS1 exhibits a ratiometric fluorescence response from sky blue to yellow colour upon the addition of Zn2+ ions with a limit of detection (LOD) of 0.05 ppm. The other metal ions such as Cu2+, Co2+ and Fe2+ demonstrate fluorescence quenching behaviour with LODs of 0.1, 0.3 and 0.7 ppm, respectively. The intramolecular charge transfer (ICT) shows the variation in TS1 emission behaviour upon metal ions interaction and quantitatively discriminates the metal ion concentrations. TS1 conferred a visual colorimetric change from colourless to magenta, enabling naked-eye detection of Fe2+ and showing clear discrimination between Fe2+ and Fe3+ ions for the real-time water samples. Furthermore, we have investigated the effect of TS1 in Zebrafish larvae/embryos and cytotoxicity in human urinary tract transitional cell carcinoma cells (UM-UC-3).

Copper ferrite nanoparticles induced cytotoxicity and oxidative stress in Channel catfish ovary cells.

Nanomaterials are the sixth most emerging contaminants that are entering into aquatic habitat posing a risk to the inhabiting organisms. Nanoparticles of copper ferrite have been extensively used in biomedical applications. However, very limited studies are available on the cytotoxicity evaluation of copper ferrite nanoparticles (CuFe2O4NPs) on different cell lines. The current work investigates on the cytotoxicity, oxidative stress and morphological variations triggered by CuFe2O4NPs in Channel catfish ovary (CCO) cells using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT), neutral red uptake (NRU), lipid peroxidation (LPO), catalase (CAT), reduced glutathione (GSH), glutathione sulfotransferase (GST) and glutathione peroxidase (GPX) assays after 24 h of treatment. Dose dependent decline in cell survival was noticed in MTT and NRU assays. A significant increase in LPO, GST and GPX was observed in CCO cells exposed to CuFe2O4NPs after 24 h of treatment. However, the CAT and GSH levels in CCO cells exposed to CuFe2O4NPs decreased significantly after 24 h. The CCO cells exposed to 10 µg/mL concentration of CuFe2O4NPs for 24 h showed remarkable changes in their morphology. Further, the study also describes the detailed mechanism of toxicity of CuFe2O4NPs in other model cell lines to probe the risk of inhabiting organisms.

Graphene oxide induces cytotoxicity and oxidative stress in bluegill sunfish cells.

Graphene oxide (GO) is considered a promising material for biological application due to its unique properties. However, the potential toxicity of GO to aquatic organism particularly bluegill sun fish cells (BF-2) is unexplored or remains poorly understood. GO-induced cytotoxicity and oxidative stress in BF-2 cells were assessed using a battery of biomarkers. Two different biological assays (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and neutral red uptake were used to evaluate the cytotoxicity of GO on BF-2 cells. It was found that GO induced dose- and time-dependent cytotoxicity on BF-2 cells. BF-2 cells exposed to lower concentration of GO (40 µg ml-1 ) for 24 induced morphological changes when compared to their respective controls. As evidence for oxidative stress lipid peroxidation, superoxide dismutase, catalase, reactive oxygen species and 8-hydroxy-2'-deoxyguanosine levels were increased and glutathione levels were found to decline in BF-2 cells after treatment with GO. Our findings demonstrate that GO when exposed to BF-2 fish cells cause oxidative stress.

Evaluation of cytotoxicity, morphological alterations and oxidative stress in Chinook salmon cells exposed to copper oxide nanoparticles.

The current study is aimed to study cytotoxicity and oxidative stress mediated changes induced by copper oxide nanoparticles (CuO NPs) in Chinook salmon cells (CHSE-214). To this end, a number of biochemical responses are evaluated in CHSE-214 cells which are as follows [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide] MTT, neutral red uptake (NRU), lactate dehydrogenase (LDH), protein carbonyl (PC), lipid peroxidation (LPO), oxidised glutathione (GSSG), reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione sulfo-transferase (GST), superoxide dismutase (SOD), catalase (CAT), 8-Hydroxy-2'-deoxyguanosine (8-OHdG) and reactive oxygen species (ROS), respectively. The 50% inhibition concentration (IC50) of CuO NPs to CHSE-214 cells after 24 h exposure was found to be 19.026 µg ml(-1). Viability of cells was reduced by CuO NPs, and the decrease was dose dependent as revealed by the MTT and NRU assay. CHSE-214 cells exposed to CuO NPs induced morphological changes. Initially, cells started to detach from the surface (12 h), followed by polyhedric, fusiform appearance (19 h) and finally the cells started to shrink. Later, the cells started losing their cellular contents leading to their death only after 24 h. LDH, PC, LPO, GSH, GPx, GST, SOD, CAT, 8-OHdG and ROS responses were seen significantly increased with the increase in the concentration of CuO NPs when compared to their respective controls. However, significant decrease in GSSG was perceptible in CHSE-214 cells exposed to CuO NPs in a dose-dependent manner. Our data demonstrated that CuO NPs induced cytotoxicity in CHSE-214 cells through the mediation of oxidative stress. The current study provides a baseline for the CuO NPs-mediated cytotoxic assessment in CHSE-214 cells for the future studies.

Assessment of cytotoxicity and oxidative stress induced by titanium oxide nanoparticles on Chinook salmon cells.

Titanium oxide nanoparticles (TiO2 NPs) have received wide attention in diverse application, but the potential impact of these nanomaterials on the environment, aquatic life and especially on fish cell lines is lacking. The present study aimed to investigate the cytotoxicity and oxidative stress induced by TiO2 NPs on Chinook salmon cells derived from Oncorhynchus tshawytscha embryos (CHSE-214). The The MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide] and neutral red (NR) assays in CHSE-214 cells exposed to TiO2 NPs revealed concentration-dependent cytotoxic effect in the range of 10 to 60 µg/ml for 24 h. CHSE-214 cells exposed to TiO2 NPs (10-60 µg/ml) exhibited significant decline in superoxide dismutase (SOD), catalase (CAT) glutathione (GSH) content and increased lipid peroxidation (LPO) in a concentration-dependent manner. TiO2 NPs induced cytotoxicity and oxidative stress in CHSE-214 cells which serve as a base line studies for future studies.

Aluminium oxide nanoparticles induced morphological changes, cytotoxicity and oxidative stress in Chinook salmon (CHSE-214) cells.

Aluminium oxide nanoparticles (Al2 O3 NPs) are increasingly used in diverse applications that has raised concern about their safety. Recent studies suggested that Al2 O3 NPs induced oxidative stress may be the cause of toxicity in algae, Ceriodaphnia dubia, Caenorhabditis elegans and Danio rerio. However, there is paucity on the toxicity of Al2 O3 NPs on fish cell lines. The current study was aimed to investigate Al2 O3 NPs induced cytotoxicity, oxidative stress and morphological abnormality of Chinnok salmon cells (CHSE-214). A dose-dependent decline in cell viability was observed in CHSE-214 cells exposed to Al2 O3 NPs. Oxidative stress induced by Al2 O3 NPs in CHSE-214 cells has resulted in the significant reduction of superoxide dismutase, catalase and glutathione in a dose-dependent manner. However, a significant increase in glutathione sulfo-transferase and lipid peroxidation was observed in CHSE-214 cells exposed to Al2 O3 NPs in a dose-dependent manner. Significant morphological changes in CHSE-214 cells were observed when exposed to Al2 O3 NPs at 6, 12 and 24 h. The cells started to detach and appear spherical at 6 h followed by loss of cellular contents resulting in the shrinking of the cells. At 24 h, the cells started to disintegrate and resulted in cell death. Our data demonstrate that Al2 O3 NPs induce cytotoxicity and oxidative stress in a dose-dependent manner in CHSE-214 cells. Thus, our current work may serve as a base-line study for future evaluation of toxicity studies using CHSE-214 cells.

Lipid peroxidation and its control in Anguilla anguilla hepatocytes under silica-coated iron oxide nanoparticles (with or without mercury) exposure.

Having multidisciplinary applications, iron oxide nanoparticles can inevitably enter aquatic system and impact inhabitants such as fish. However, the studies in this context have ignored the significance of obvious interaction of iron oxide nanoparticles with other persistent co-contaminants such as mercury (Hg) in the modulation of the toxicity and underlying mechanisms of iron oxide nanoparticles and Hg alone, and concomitant exposures. This study aimed to evaluate lipid peroxidation (LPO) and its control with glutathione (GSH) and associated enzymes (such as glutathione reductase, GR; glutathione peroxidase, GPX; glutathione sulfo-transferase, GST) in European eel (Anguilla anguilla L.) hepatocytes exposed to stressors with following schemes: (i) no silica-coated iron oxide nanoparticles functionalized with dithiocarbamate (Fe3O4@SiO2/Si DTC, hereafter called 'FeNPs'; size range 82 ± 21 to 100 ± 30 nm) or Hg, (ii) FeNPs (2.5 µg L(-1)) alone, (iii) Hg (50 µg L(-1)) alone and (iv) FeNPs + Hg concomitant condition during 0 to 72 h. The exhibition of a differential coordination between GSH regeneration (determined as GR activity) and GSH metabolism (determined as the activity of GPX and GST) was perceptible in A. anguilla hepatocytes in order to control FeNPs, Hg and FeNPs + Hg exposure condition-mediated LPO. This study revealed the significance of a fine tuning among GR, GPX and GST in keeping LPO level under control during FeNPs or Hg alone exposure, and a direct role of total GSH (TGSH) in the control of LPO level and impaired GSH metabolism under the concomitant (FeNPs + Hg) exposure. An interpretation of the fish risk to FeNPs in a multi-pollution state should equally consider the potential outcome of the interaction of FeNPs with other contaminants.

Modulation of glutathione and its dependent enzymes in gill cells of Anguilla anguilla exposed to silica coated iron oxide nanoparticles with or without mercury co-exposure under in vitro condition.

The current study aimed to investigate the modulation of glutathione (GSH) and its dependent enzymes (glutathione reductase, GR; glutathione peroxidase, GPx; glutathione sulfotransferase, GST) from 0 to 72 h in the gill cells of Anguilla anguilla under in vitro condition exposed to silica coated iron oxide nanoparticles functionalized with dithiocarbamate (Fe3O4@SiO2/SiDTC, hereafter called 'IONPs'; 100 nm; 2.5 mgL(-1)) with or without mercury (Hg) coexposure. Significantly decreased TGSH content under IONP alone exposure from 0 to 72 h indicated increased utilization of the TGSH in response to IONP stress. Significant increases in the activity of GR, GPx and GST were depicted when exposed to IONP alone. Lipid peroxidation (LPO), a membrane damage trait also significantly increased under IONP alone exposure indicating the efficient role of antioxidant induction abolishing the IONP-mediated enhanced reactive oxygen species. Under Hg exposure, gill cells displayed significantly increased activity of the studied enzymes (GR, GPx and GST) and LPO which was accompanied by significantly decreased TGSH content. Concomitant (IONPs+Hg) exposure displayed a synergistic response to that of individual responses of either IOPN or Hg which was evident by significant increases in GR, GPx, GST and LPO. Overall, our findings revealed a fine tuning among the GSH and its dependent enzyme modulation under IONP, Hg and its concomitant (IONPs+Hg) exposure in A. anguilla gill cells under in vitro condition.

Brain glutathione redox system significance for the control of silica-coated magnetite nanoparticles with or without mercury co-exposures mediated oxidative stress in European eel (Anguilla anguilla L.).

This in vitro study investigates the impact of silica-coated magnetite particles (Fe3O4@SiO2/SiDTC, hereafter called IONP; 2.5 mg L(-1)) and its interference with co-exposure to persistent contaminant (mercury, Hg; 50 µg L(-1)) during 0, 2, 4, 8, 16, 24, 48, and 72 h on European eel (Anguilla anguilla) brain and evaluates the significance of the glutathione (GSH) redox system in this context. The extent of damage (membrane lipid peroxidation, measured as thiobarbituric acid reactive substances, TBARS; protein oxidation, measured as reactive carbonyls, RCs) decreased with increasing period of exposure to IONP or IONP + Hg which was accompanied with differential responses of glutathione redox system major components (glutathione reductase, GR; glutathione peroxidase, GPX; total GSH, TGSH). The occurrence of antagonism between IONP and Hg impacts was evident at late hour (72 h), where significantly decreased TBARS and RC levels and GR and glutathione sulfo-transferase (GST) activity imply the positive effect of IONP + Hg concomitant exposure against Hg-accrued negative impacts [vs. early (2 h) hour of exposure]. A period of exposure-dependent IONP alone and IONP + Hg joint exposure-accrued impact was perceptible. Additionally, increased susceptibility of the GSH redox system to increased period of exposure to Hg was depicted, where insufficiency of elevated GR for the maintenance of TGSH required for membrane lipid and cellular protein protection was displayed. Overall, a fine-tuning among brain glutathione redox system components was revealed controlling IONP + Hg interactive impacts successfully.

Plasmatocyte-spreading peptide influences hemocyte behavior via eicosanoids.

Hemocyte-spreading behavior is required for expressing a cellular immune response, nodulation, which clears the vast majority of invading microbes from circulation. The nodulation response is completed by a layer of plasmatocytes, which spread over the nodule and initiate a malanization process leading to darkened nodules. Plasmatocyte-spreading peptide (PSP), the first reported insect cytokine, is responsible for mediating the spreading and attachment of some subclasses of plasmatocytes to nodules. Prostaglandins (PGs), one group of eicosanoids formed from arachidonic acid (AA), also mediate plasmatocyte spreading (PS), although the potential interactions between the PSP and PG signal transduction pathways have not been investigated. We tested our hypothesis that PSP acts via biosynthesis of eicosanoids, specifically PGs, in the beet armyworm, Spodoptera exigua. In this study, we report that (1) PSP and PGE(2) independently stimulated Ca(++)-dependent PS, (2) inhibitors of PG biosynthesis reversibly blocked PS, (3) dsRNA silencing the gene encoding proPSP blocked PS, which was rescued by PSP and by AA, (4) PSP-stimulated PS was reversibly impaired by inhibitors of PG biosynthesis, and (5) the inhibitor-impaired spreading was rescued by AA. Taken together, these points strongly support our model showing that PSP acts via a plasmatocyte-surface receptor, which stimulates biosynthesis of the PGs responsible for mediating plasmatocytes spreading.