Intestinal Brush Border Research Articles

Oral peptide drug delivery: design of SEDDS providing a protective effect against intestinal membrane-bound enzymes.

This study presents an emerging approach for oral peptide drug delivery by designing self-emulsifying drug delivery systems (SEDDS) capable of protecting peptide drugs from intestinal brush border membrane-bound (BBM) enzymes. Tuftsin was incorporated as a model peptide into three optimized SEDDS formulations through hydrophobic ion pairing with the anionic surfactants docusate (AOT), N-octadecyl sulfate (OS), and lauryl sulfate (LS). SEDDS- 1 consisted of octyldodecanol, polyoxyethylene (10) oleyl ether, polyoxyethylene (20) oleyl ether and citronellol. SEDDS- 2 were formulated with isopropylmyristate, polyoxyethylene (20) oleyl ether and eugenol. SEDDS- 3 included caprylic acid, PEG- 35 castor oil and citronellol. The resulting nanoemulsions were characterized for droplet size, zeta potential, polydispersity index (PDI), and stability in biorelevant media. Enzymatic degradation studies with aminopeptidase N and ex vivo rat small intestine revealed remarkable protective effects. SEDDS- 3 exhibited superior performance, preserving over 80% of tuftsin after 4h, followed by SEDDS- 2 protecting 70% of tuftsin, while the unformulated peptide was entirely degraded within 20 min. Furthermore, SEDDS- 2 demonstrated enhanced permeation of tuftsin across intestinal mucosa by achieving a 4-fold increase, while SEDDS- 3 led to a 3-fold enhancement in permeation compared to the unformulated peptide. Accordingly, SEDDS- 3 demonstrates the greatest potential for peptide delivery due to its superior protective performance and enhanced permeation compared to the control. These findings underscore the potential of SEDDS as a versatile platform for safeguarding peptide drugs against enzymatic degradation in the intestinal environment. By modifying their composition, SEDDS can unlock new possibilities for efficient oral peptide drug delivery, overcoming critical enzymatic and mucosal barriers.

Disaccharidase Enzyme Deficiency in Adult Patients With Gas and Bloating.

Disaccharidases produced by the small intestinal brush border facilitate digestion of dietary carbohydrates. If deficient, they can cause carbohydrate malabsorption, resulting in several abdominal symptoms. Our aim was to examine the prevalence of disaccharidase deficiency and correlate this with abdominal symptoms in adult patients with chronic abdominal symptoms. In a retrospective study, patients with gas and bloating and normal endoscopy and computed tomography scan were assessed for lactase, sucrase, maltase, palatinase, and glucoamylase activity. Nine common symptoms such as pain, cramping, constipation, belching, bloating, fullness, indigestion, nausea, diarrhea, vomiting, and gas were assessed for their frequency, intensity, and duration using a validated scale, and a total symptom index was calculated and compared. K-means cluster analysis was performed on lactase-deficient and pandeficient patients with deficiency in 3 or more enzymes. Four hundred ninety-six patients (78.4% female) were enrolled of whom 143 (28.8%) had single enzyme deficiency, 9 (1.8%) had double enzyme deficiency, and 48 (9.7%) were pandeficient. The mean symptom prevalence and its severity were not significantly different between those with or without disaccharidase deficiency. Patients with pandeficiency did not have worse symptoms than those with single or double enzyme deficiency. No single symptom was more prevalent in patients with confirmed enzyme deficiency than those without. Three groups were identified in cluster analysis of pandeficient patients with one group demonstrating significantly lower average symptoms of cramping, indigestion, and nausea. Disaccharidase deficiency is common in adults presenting with gas, bloating, distention, and pain. Because these deficiencies are treatable with enzyme supplements or diet, an evaluation for disaccharidase deficiency should be routinely considered.

Skim Milk Culture of Lactobacillus johnsonii SBT0309 Increases Intestinal Alkaline Phosphatase Activity and Inhibits Lipopolysaccharide-Induced Interleukin-8 Production in Intestinal Epithelial Cells.

Intestinal alkaline phosphatase (IAP) is an enzyme expressed in the intestinal brush border, which may exert anti-inflammatory effects by detoxifying lipopolysaccharides (LPSs), thereby preventing metabolic disorders. Various food components have been reported to influence IAP activity. However, few studies have evaluated the effects of fermented milk on IAP activity. In this study, we aimed to investigate fermented milk with high IAP-activating capacity and investigate its effect. We screened a skim milk culture (SC), a fermented milk model, using differentiated Caco-2 cells. We investigated the effect of SC on IAP activity and gene expression in the Drosophila midgut. Quantitative PCR and immunoblot assays were conducted to examine gene and protein levels. Among the SC samples from different lactic acid bacteria or bifidobacteria, the SC of Lactobacillus johnsonii SBT0309 (LJ0309 SC) demonstrated a particularly strong capacity to activate IAP in Caco-2 cells, demonstrated by significantly increased IAP gene expression and protein levels in Caco-2 cells. Additionally, LJ0309 SC inhibited increased secretion of IL-8 in LPS-stimulated Caco-2 cells. Finally, in Drosophila melanogaster fed LJ0309 SC, we observed an increase in both IAP activity and gene expression in the midgut. LJ0309 SC increased IAP activity and gene expression in both Caco-2 cells and the Drosophila midgut, and inhibited the inflammatory response in LPS-stimulated Caco-2 cells. Although further in vivo studies are required, LJ0309 SC might help to ameliorate LPS-induced inflammation and disease via IAP activation.

Review Article: Novel Enzyme Therapy Design for Gluten Peptide Digestion Through Exopeptidase Supplementation.

Dietary peptides are increasingly linked to inflammatory gastrointestinal diseases, exemplified by coeliac disease. Coeliac disease is caused by an acquired immune response to proline- and glutamine-rich gluten peptides, which bottleneck proteolysis and provide substrates for immune recognition. Enzyme therapies aim to eliminate gluten immunogenic peptides as an adjunct to gluten-free diet. To investigate overlooked aspects of enzyme development given difficulties in translating preclinical efficacy into clinical benefit. We assessed mode-of-action, target organ and drug delivery in the context of digestive physiology and motility for gluten-digesting enzymes on the market or in development until 1 December 2024. Most enzymes were gastric endopeptidases specific for proline or glutamine residues. Gastric enzymes may achieve poor enzyme-substrate exposure due to limited mixing and rapid emptying of water-soluble particles. Moreover, endopeptidases cleave proteins/peptides into shorter peptides but do not systematically cleave protein into absorbable fractions. Natural digestive physiology provides thorough mixing at the intestinal brush border, which produces exopeptidases necessary to fully digest proline-rich peptides. Despite reduced activity in patients with coeliac disease, exopeptidases remain underexplored as therapeutic agents. Given limited substrate scope and end-to-end digestion, exopeptidases are ineffective as single agents, requiring functional combinations. Furthermore, vulnerability to gastric acid requires stabilisation or formulation for rapid enteric release. Enzymes should be stabilised throughout the gastrointestinal tract including the small intestine. Exopeptidases perform a critical function by systematically generating absorbable fractions, warranting future investigation as therapeutic agents. Sensitive and translational biomarkers are needed to better assess enzyme efficacy in real-meal conditions.

Grape Pomace as a Source of Phenolics for the Inhibition of Starch Digestion Enzymes: A Comparative Study and Standardization of the Efficacy.

The increase in the incidence of hyperglycemia and diabetes poses the challenge of finding cost-effective natural inhibitors of starch digestion enzymes. Among natural compounds, phenolics have been considered as promising candidates. The aims of this study were as follows: (a) to investigate the effectiveness of the inhibition of different winemaking byproducts towards intestinal brush border α-glucosidase and pancreatic α-amylase in vitro; (b) to calculate an efficacy index relative to the standard acarbose for the phenolic pool of winemaking byproducts, as well as for isolated phenolic compounds and for the phenolic pools of different plants studied in the literature, in order to rank winemaking byproducts with respect to the reference drug and other natural alternatives. Among winemaking byproducts, red grape skins showed the highest inhibitory activities towards both α-glucosidase and α-amylase, which were, on average, 4.9 and 2.6 µg acarbose equivalents/µg total phenolics (µg Ac eq/µg GAE), respectively. A correlation was observed between the total phenolic contents of red grape skins and their inhibitory effectiveness, which is useful for standardizing the efficacy of phenolic extracts obtained from different winemaking processes. In general, the inhibitory activity of the phenolic pool of grape skins was higher than those of isolated phenolic compounds, namely anthocyanins and monomeric and polymeric flavanols and flavonols, probably due to synergistic effects among compounds. Hence, bioactive phenolic fractions could be produced with the focus on functionality rather than purity, in line with the principles of sustainable processing. Based on the efficacy index developed to compare different phenolic compounds and phenolic-rich plants studied in the literature as starch digestion enzyme inhibitors, red grape skins proved to be cost-effective candidates.

Rat small intestine extract as a source of mammalian α- and β-glycosidases to study polyphenol bioaccessibility and deglycosylation in vitro: A case study with matrix-devoid and matrix-defined apple fractions

Most polyphenols are glycosylated, affecting their uptake, metabolism, and biological activity. However, the attached sugar must be removed before absorption and functionality can take place. Yet, despite the biological and chemical implications of polyphenol (de-)glycosylation, most in vitro digestion assays omit the utilization of intestinal brush border α- and/or β-glycosidases to study polyphenol bioaccessibility and deglycosylation. This study investigated the effect of rat small intestine extract (RSIE) as an affordable source of mammalian α- and β-glycosidases in different food matrices: matrix-devoid whole apple extract, whole apple, apple juice, and apple pomace. Using the INFOGEST 2.0 model, transepithelial polyphenol absorption, UHPLC-ESI-QTOF-MS/MS, and the inclusion of RSIE at the 15 U*mL−1 maltase activity reported in the human epithelium, the role of RSIE in polyphenol bioaccessibility and deglycosylation was explored. Moreover, the effect of the plant cell wall (PCW) matrix on the role of RSIE was mechanistically investigated by comparing whole apple (or pomace) with their respective extracts. 36 glycosylated polyphenols were identified, including 33 β-O-glycosides and 3 α-O-glycosides. The content of bioaccessible polyphenol β-O-glycosides and α-O-glycosides was significantly lower (p < 0.001) when RSIE was present, which resulted in a concomitant generation of the aglycone forms (phloretin, quercetin, ferulic acid, caffeic acid and p-coumaric acid). However, the concentration of aglycones was much lower than the reduction in the concentration of glycosylated polyphenols, strongly suggesting that polyphenols bind to RSIE. Matrix-devoid whole apple extract, or pomace extract, exhibited higher polyphenol bioaccessibility than whole apple or pomace, likely due to reduced interactions between polyphenols and the food matrix. Importantly, these differences in bioaccessibility diminished with RSIE, suggesting that RSIE α-glycosidases cleaved α-glucans and disrupted the PCW structure.

Intestinal Epithelial Cell Brush Border Membrane Cl:HCO3 Exchanger Regulation by Mast Cells in Chronic Ileitis.

Malabsorption of NaCl is the primary cause of diarrhea in inflammatory bowel disease (IBD). Coupled NaCl absorption occurs via the dual operation of Na:H and Cl:HCO3 exchange in the brush border membrane (BBM) of villus cells. Cl:HCO3 exchange is mediated by BBM transporters DRA (downregulated in adenoma) and PAT1 (putative anion transporter 1) in the mammalian small intestine. DRA/PAT1-mediated Cl:HCO3 exchange was significantly downregulated in the BBM of villus cells in a rabbit model of chronic ileitis, while Na:H exchange was unaffected. The inhibition of Cl:HCO3 exchange was restored in the rabbits when treated with a broad-spectrum immunomodulator, i.e. a glucocorticoid, indicating that the downregulation of DRA/PAT1 is likely to be immune-mediated during chronic enteritis. Mucosal mast cells are one type of key immune cells that are known to proliferate and release immune inflammatory mediators, thus playing a significant role in the pathogenesis of IBD. However, how mast cells may regulate DRA- and PAT1-mediated Cl:HCO3 exchange in a rabbit model of chronic ileitis is unknown. In this study, treatment of rabbits with chronic intestinal inflammation with the mast cell stabilizer ketotifen did not affect the mucosal architecture of the inflamed intestine. However, ketotifen treatment reversed the inhibition of Cl:HCO3 activity in the BBM of villus cells. This restoration of Cl:HCO3 activity to normal levels by ketotifen was found to be secondary to restoring the affinity of the exchangers for its substrate chloride. This observation was consistent with molecular studies, where the mRNA and BBM protein expressions of DRA and PAT1 remained unaffected in the villus cells under all experimental conditions. Thus, this study indicates that mast cells mediated the inhibition of coupled NaCl absorption by inhibiting Cl:HCO3 exchange in a rabbit model of chronic enteritis.

Polyphenols from unconventional fruit by-products protect human epithelial intestinal cells from oxidative damage

Polyphenols from unconventional fruit by-products protect human epithelial intestinal cells from oxidative damage

Exopeptidase combination enhances the degradation of isotopically labelled gluten immunogenic peptides in humans.

Celiac disease is a common autoimmune-like enteropathy caused by an aberrant response to incompletely digested dietary gluten. Gluten immunogenic peptides including the immunodominant 33-mer are thought to be resistant to proteolytic digestion by human gastrointestinal peptidases. We developed a novel enzyme therapy approach to support gluten peptide digestion using a combination of two tandem-acting exopeptidases, AMYNOPEP, that complement the intrinsic enzymatic activity of intestinal brush border enterocytes. We evaluated the effects of AMYNOPEP supplementation on 33-mer degradation in vitro and in vivo. In a cross-over clinical study, healthy volunteers with no gastrointestinal disorders were given stable isotope (SI) labelled 33-mer peptides in the presence of varying peptide substrates and caloric loads, with and without AMYNOPEP. 33-mer degradation products (SI-labelled single amino acids) were measured in the blood plasma using LC-MS/MS. AMYNOPEP achieved rapid, complete amino-to-carboxyl terminal degradation of the 33-mer in vitro, generating single amino acids and dipeptides. In healthy volunteers, AMYNOPEP supplementation significantly increased 33-mer degradation and absorption of SI-labelled amino acids even in the presence of competing substrates. Specifically, we observed a 2.8-fold increase in the Cmax of stable isotope-labelled amino acids in the presence of wheat gluten. The absorption kinetics of labelled amino acids derived from 33-mer digestion with AMYNOPEP closely resembled that of SI-labelled X-Proline dipeptides administered without enzyme supplementation, highlighting the rapid hydrolytic activity of AMYNOPEP on polypeptides. AMYNOPEP achieved complete degradation of the 33-mer into single amino acids and dipeptides in vitro and significantly improved 33-mer degradation kinetics in healthy volunteers, as measured by labelled amino acid detection, warranting further investigation into the potential therapeutic benefits of exopeptidase combinations for patients with gluten-related health disorders including celiac disease.

Daily rhythm in feeding behavior and digestive processes in totoaba (Totoaba macdonaldi) under commercial farming conditions

Daily rhythm in feeding behavior and digestive processes in totoaba (Totoaba macdonaldi) under commercial farming conditions

Identification of Antioxidant Methyl Derivatives of Ortho-Carbonyl Hydroquinones That Reduce Caco-2 Cell Energetic Metabolism and Alpha-Glucosidase Activity.

α-glucosidase, a pharmacological target for type 2 diabetes mellitus (T2DM), is present in the intestinal brush border membrane and catalyzes the hydrolysis of sugar linkages during carbohydrate digestion. Since α-glucosidase inhibitors (AGIs) modulate intestinal metabolism, they may influence oxidative stress and glycolysis inhibition, potentially addressing intestinal dysfunction associated with T2DM. Herein, we report on a study of an ortho-carbonyl substituted hydroquinone series, whose members differ only in the number and position of methyl groups on a common scaffold, on radical-scavenging activities (ORAC assay) and correlate them with some parameters obtained by density functional theory (DFT) analysis. These compounds' effect on enzymatic activity, their molecular modeling on α-glucosidase, and their impact on the mitochondrial respiration and glycolysis of the intestinal Caco-2 cell line were evaluated. Three groups of compounds, according their effects on the Caco-2 cells metabolism, were characterized: group A (compounds 2, 3, 5, 8, 9, and 10) reduces the glycolysis, group B (compounds 1 and 6) reduces the basal mitochondrial oxygen consumption rate (OCR) and increases the extracellular acidification rate (ECAR), suggesting that it induces a metabolic remodeling toward glycolysis, and group C (compounds 4 and 7) increases the glycolysis lacking effect on OCR. Compounds 5 and 10 were more potent as α-glucosidase inhibitors (AGIs) than acarbose, a well-known AGI with clinical use. Moreover, compound 5 was an OCR/ECAR inhibitor, and compound 10 was a dual agent, increasing the proton leak-driven OCR and inhibiting the maximal electron transport flux. Additionally, menadione-induced ROS production was prevented by compound 5 in Caco-2 cells. These results reveal that slight structural variations in a hydroquinone scaffold led to diverse antioxidant capability, α-glucosidase inhibition, and the regulation of mitochondrial bioenergetics in Caco-2 cells, which may be useful in the design of new drugs for T2DM and metabolic syndrome.

Monobutyrin Can Regulate the Gut Microbiota, Which Is Beneficial for the Development of Intestinal Barrier Function and Intestinal Health in Weaned Mice.

In this study, we investigated the effect of monobutyrin (MB) on the gut microbiota and intestinal health of weaned mice. MB was administered via gavage to 21-day-old weaned mice. Samples of small intestinal and ileal contents were collected on day 1, day 7, and day 21 post-administration. Seven days of MB administration enhanced the mucin layer and morphological structure of the intestine and the integrity of the intestinal brush border. Both MB and sodium butyrate (SB) accelerated tight junction development. Compared to SB, MB modulated intestinal T cells in a distinct manner. MB increased the ratio of Treg cells in the small intestine upon the cessation of weaning. After 21 days of MB administration, enhancement of the villus structure of the ileum was observed. MB increased the proportion of Th17 cells in the ileum. MB facilitated the transition of the small intestinal microbiota toward an adult microbial community structure and enhanced the complexity of the microbial community structure. An increase in Th17 cells enhanced intestinal barrier function. The regulatory effect of MB on Th17 cells may occur through the intestinal microbiota. Therefore, MB can potentially be used to promote intestinal barrier function, especially for weaning animals, with promising application prospects.

CGMP-dependent kinase 2, Na+/H+ exchanger NHE3, and PDZ-adaptor NHERF2 co-assemble in apical membrane microdomains.

Trafficking, membrane retention, and signal-specific regulation of the Na+/H+ exchanger 3 (NHE3) are modulated by the Na+/H+ Exchanger Regulatory Factor (NHERF) family of PDZ-adapter proteins. This study explored the assembly of NHE3 and NHERF2 with the cGMP-dependent kinase II (cGKII) within detergent-resistant membrane microdomains (DRMs, "lipid rafts") during in vivo guanylate cycle C receptor (Gucy2c) activation in murine small intestine. Small intestinal brush border membranes (siBBMs) were isolated from wild type, NHE3-deficient, cGMP-kinase II-deficient, and NHERF2-deficient mice, after oral application of the heat-stable Escherichia coli toxin (STa) analog linaclotide. Lipid raft and non-raft fractions were separated by Optiprep density gradient centrifugation of Triton X-solubilized siBBMs. Confocal microscopy was performed to study NHE3 redistribution after linaclotide application in vivo. In the WT siBBM, NHE3, NHERF2, and cGKII were strongly raft associated. The raft association of NHE3, but not of cGKII, was NHERF2 dependent. After linaclotide application to WT mice, lipid raft association of NHE3 decreased, that of cGKII increased, while that of NHERF2 did not change. NHE3 expression in the BBM shifted from a microvillar to a terminal web region. The linaclotide-induced decrease in NHE3 raft association and in microvillar abundance was abolished in cGKII-deficient mice, and strongly reduced in NHERF2-deficient mice. NHE3, cGKII, and NHERF2 form a lipid raft-associated signal complex in the siBBM, which mediates the inhibition of salt and water absorption by Gucy2c activation. NHERF2 enhances the raft association of NHE3, which is essential for its close interaction with the exclusively raft-associated activated cGKII.

Glucose stockpile in the intestinal apical brush border in C. elegans

Glucose stockpile in the intestinal apical brush border in C. elegans

Pyroptosis Tuning in Intestinal Cryptosporidiosis via the Natural Histone Deacetylase Inhibitor Romidepsin.

Cryptosporidium is an opportunistic protozoan, with many species of cross-human infectivity. It causes life-threatening diarrhoea in children and CD4-defective patients. Despite its limited efficacy, nitazoxanide remains the primary anti-cryptosporidial drug. Cryptosporidium infects the intestinal brush border (intracellular-extracytoplasmic) and down-regulates pyroptosis to prevent expulsion. Romidepsin is a natural histone deacetylase inhibitor that triggers pyroptosis. Romidepsin's effect on cryptosporidiosis was assessed in immunocompromised mice via gasdermin-D (GSDM-D) immunohistochemical expression, IFN-γ, IL-1β and IL-18 blood levels by ELISA, and via parasite scanning by modified Ziehl-Neelsen staining and scanning electron microscopy (SEM). Oocyst deformity and local cytokines were also assessed in ex vivo ileal explants. Following intraperitoneal injection of romidepsin, oocyst shedding significantly reduced at the 9th, 12th and 15th d.p.i. compared with infected-control and drug-control (nitazoxanide-treated) mice. H&E staining of intestinal sections from romidepsin-treated mice showed significantly low intestinal scoring with marked reduction in epithelial hyperplasia, villous blunting and cellular infiltrate. SEM revealed marked oocyst blebbing and paucity (in vivo and ex vivo) after romidepsin compared with nitazoxanide. Regarding pyroptosis, romidepsin triggered significantly higher intestinal GSDM-D expression in vivo, and higher serum/culture IFN-γ, IL-1β and IL-18 levels in romidepsin-treated mice than in the control groups. Collectively, in cryptosporidiosis, romidepsin succeeded in enhancing pyroptosis in the oocysts and infected epithelium, reducing infection and shifting the brush border towards normalisation.

Role of sodium octanoate in regulating survival, growth, intestinal development, digestive and absorptive capacities, antioxidant capacity and innate immunity of large yellow croaker (Larimichthys crocea) larvae

Role of sodium octanoate in regulating survival, growth, intestinal development, digestive and absorptive capacities, antioxidant capacity and innate immunity of large yellow croaker (Larimichthys crocea) larvae

Aster-dependent nonvesicular transport facilitates dietary cholesterol uptake.

Intestinal absorption is an important contributor to systemic cholesterol homeostasis. Niemann-Pick C1 Like 1 (NPC1L1) assists in the initial step of dietary cholesterol uptake, but how cholesterol moves downstream of NPC1L1 is unknown. We show that Aster-B and Aster-C are critical for nonvesicular cholesterol movement in enterocytes. Loss of NPC1L1 diminishes accessible plasma membrane (PM) cholesterol and abolishes Aster recruitment to the intestinal brush border. Enterocytes lacking Asters accumulate PM cholesterol and show endoplasmic reticulum cholesterol depletion. Aster-deficient mice have impaired cholesterol absorption and are protected against diet-induced hypercholesterolemia. Finally, the Aster pathway can be targeted with a small-molecule inhibitor to manipulate cholesterol uptake. These findings identify the Aster pathway as a physiologically important and pharmacologically tractable node in dietary lipid absorption.

Analysis of Synergism between Extracellular Polysaccharide from Bacillus thuringensis subsp. kurstaki HD270 and Insecticidal Proteins.

Bacillus thuringiensis (Bt) is the most widely used biopesticide worldwide and can produce several insecticidal crystal proteins and vegetative insecticidal proteins (Vips) at different growth stages. In our previous study, extracellular polysaccharides (EPSs) of Bt strain HD270 were found to enhance the insecticidal activity of Cry1Ac protoxin against Plutella xylostella (L.) and promote the binding of Cry1Ac to the intestinal brush border membrane vesicles (BBMVs). Whether the synergistic activity of Bt EPSs is common to other Cry1-type or Vip proteins is unclear, as is the potential synergistic mechanism. In this study, crude EPS-HD270 was found to increase the toxicity of Cry1-type toxins and Vip3Aa11 against different lepidopteran pests by approximately 2-fold. The purified EPS-HD270 also possessed synergistic activity against the toxicity of Cry1Ac and Vip3Aa11 against Spodoptera frugiperda (J.E. Smith) and Helicoverpa armigera (Hübner). Furthermore, we found that EPS-HD270 had a strong binding ability with Vip3Aa11 and promoted the binding of Vip3Aa11 to the BBMVs of H. armigera and S. frugiperda. Bt EPS-HD270 also protected Vip3Aa11 from proteolytic processing in larval midgut juice. Bt EPSs had universal synergistic effects on Cry1-type or Vip toxins against S. frugiperda and H. armigera. Bt EPS-HD270 exhibited synergistic activity with Vip3Aa through promotion of binding to BBMVs and protection from digestion by midgut protease. The results indicated that synergistic activity with Bt toxins was an important function of Bt EPSs, which was very different from other Bacillus spp.

Adverse Effect of Metallic Gold and Silver Nanoparticles on Xenopus laevis Embryogenesis.

Exposure to metal nanoparticles is potentially harmful, particularly when occurring during embryogenesis. In this study, we tested the effects of commercial AuNPs and AgNPs, widely used in many fields for their features, on the early development of Xenopus laevis, an anuran amphibian key model species in toxicity testing. Through the Frog Embryo Teratogenesis Assay-Xenopus test (FETAX), we ascertained that both nanoparticles did not influence the survival rate but induced morphological anomalies like modifications of head and branchial arch cartilages, depigmentation of the dorsal area, damage to the intestinal brush border, and heart rate alteration. The expression of genes involved in the early pathways of embryo development was also modified. This study suggests that both types of nanoparticles are toxic though nonlethal, thus indicating that their use requires attention and further study to better clarify their activity in animals and, more importantly, in humans.

Regulation of survival, growth performance, and intestinal health of large yellow croaker (Larimichthys crocea) larvae by sodium decanoate supplementation

Regulation of survival, growth performance, and intestinal health of large yellow croaker (Larimichthys crocea) larvae by sodium decanoate supplementation