Modulation Of Enzyme Activity Research Articles

Exposure to spaceflight enhances the virulence of Purpureocillium lilacinum against Tetranychus cinnabarinus: modulation of the host's enzyme activities and microbiome.

Multiple studies have been conducted to investigate the impact of space conditions on human, plant, and microbial life. This research investigated the virulence of spaceflight mutants of the entomopathogenic fungus Purpureocillium lilacinum (HP7, HP36, HP52) and its original strain (SP535) against Tetranychus cinnabarinus as well as examination of the T. cinnabarinus immune response, including alterations in enzyme profiles and microbiome composition post fungal application. Our observations revealed contrasting, time-specific differences in pathogenicity and tissue infection between the ground-based isolate and spaceflight mutant isolates. Analysis of detoxifying and antioxidant enzymes showed a significant reduction in enzyme activities T. cinnabarinus infected with the most virulent spaceflight mutants at 36h post-fungal infection, compared to ground-based isolates. Additionally, the microbiota was reduced due to a fungal infection, partly due to decreased antioxidant enzyme activities. Our findings indicate that changes in the microbiota of T. cinnabarinus following infection with P. lilacinum (both ground-based and spaceflight mutant isolates) resulted in variations in metabolism and genetic information-related KEGG pathways. This data can help identify potential changes in the host immune system that drive increased virulence after spaceflight mutation.

Inhibition of chondroitin sulphate-degrading enzyme Chondroitinase ABC by dextran sulphate.

Chondroitin sulphate (CS) is a sulphated glycosaminoglycan (GAG) polysaccharide found on proteoglycans (CSPGs) in extracellular and pericellular matrices. Chondroitinase ABC (CSase ABC) derived from Proteus vulgaris is an enzyme that has gained attention for the capacity to cleave chondroitin sulphate (CS) glycosaminoglycans (GAG) from various proteoglycans such as Aggrecan, Neurocan, Decorin etc. The substrate specificity of CSase ABC is well-known for targeting various structural motifs of CS chains and has gained popularity in the field of neuro-regeneration by selective degradation of CS GAG chains. Within this context, our investigation into the biochemistry of CSase ABC led us to a previously unreported inhibition of CSase ABC activity by Dextran Sulphate (DexS). To understand the inhibitory effects of DexS, we compared its inhibition of CSase ABC to that of other polysaccharides such as Heparan Sulphate, Heparin, Colominic Acid, Fucoidan, and Dextran. This analysis identified key structural factors such as monosaccharide composition and linkage, sulphation degree and overall charge as influencing CSase ABC inhibition. Remarkably, DexS emerged as a unique inhibitor of CSase ABC, with distinctive inhibitory effects that correlate with its chain length. DexS has been used to reliably induce ulcerative colitis in mice, effectively mimicking inflammatory bowel diseases in humans, and has been previously shown to inhibit both RNA polymerase and reverse transcriptase. Our investigation emphasizes the interplay between the properties of DexS and CSase ABC, providing significant insights into the utilization of polysaccharide-based inhibitors for modulating enzyme activity.

Posttranslational modifications in cardiac metabolic remodeling mediated by metabolites: Implications for disease pathology and therapeutic potential.

The nonenergy-producing or biomass-accumulating functions of metabolism are attracting increasing attention, as metabolic changes are gaining importance as discrete signaling pathways in modulating enzyme activity and gene expression. Substantial evidence suggests that myocardial metabolic remodeling occurring during diabetic cardiomyopathy, heart failure, and cardiac pathological stress (e.g., myocardial ischemia, pressure overload) contributes to the progression of pathology. Within the rewired metabolic network, metabolic intermediates and end-products can directly alter protein function and/or regulate epigenetic modifications by providing acyl groups for posttranslational modifications, thereby affecting the overall cardiac stress response and providing a direct link between cellular metabolism and cardiac pathology. This review provides a comprehensive overview of the functional diversity and mechanistic roles of several types of metabolite-mediated histone and nonhistone acylation, namely O-GlcNAcylation, lactylation, crotonylation, β-hydroxybutyrylation, and succinylation, as well as fatty acid-mediated modifications, in regulating physiological processes and contributing to the progression of heart disease. Furthermore, it explores the potential of these modifications as therapeutic targets for disease intervention.

Adverse effects of environmentally relevant microplastics on in vivo endpoints, oxidative stress, and mitogen-activated protein kinase signaling pathway and multixenobiotic resistance system in the marine rotifer Brachionus plicatilis.

This study compared the toxicological effects of environmentally relevant microplastics (MPs) on the marine rotifer Brachionus plicatilis, focusing on MPs derived from various sources, including fossil fuel-based low-density polyethylene, bio-based polylactic acid (PLA), biodegradable poly(butylene adipate-co-terephthalate), and a novel PLA modified with β-cyclodextrin. We assessed in vivo effects such as reproductive output and mortality, alongside in vitro oxidative stress responses, including oxidative stress, antioxidant enzyme activities, and activation of the mitogen-activated protein kinase (MAPK) signaling pathway and the multixenobiotic resistance (MXR) system. Reproductive output and lifespan reduced significantly across all MP types, ranging from 0.5 to 10mgL-1, indicating compromised reproductive fitness and life maintenance. At an environmentally relevant concentration of 0.5mgL-1, in vitro assessments revealed differential modulation of reactive oxygen species levels and antioxidant enzyme activities, contingent upon the specific MP type. Moreover, MAPK signaling pathway and MXR assays showed changes in phosphorylation and detoxification proteins depending on the type of MPs. This study highlights the ecological risks that various MPs, including bio-based, biodegradable, and petrochemical-based MPs, could pose in marine environments.

Rare Earth Elements Induce Drought Tolerance in Dicranopteris pedata from Ion-Adsorbed Rare Earth Mining Area in Southern China

The ion adsorption rare earth (IARE) mining areas in southern China frequently experience severe seasonal drought, posing significant challenges to plant growth. This study investigates the hypothesis that rare earth elements (REEs) present in these mining areas induce drought resistance in Dicranopteris pedata (D. pedata). An experiment was designed with three drought stress intensities (0%, 5%, and 10% PEG6000) and three levels of rare earth element (REE) addition (none, low, and high). After 72 h of drought stress, physiological indices and metabolomic profiles of D. pedata were examined. The results showed that under drought conditions, the REE additions increased the catalase and peroxidase activities of D. pedata by 99.04% and 81.25%, respectively, and the contents of proline, soluble proteins, and soluble sugars by 97.52%, 71.24%, and 61.81%, respectively. Metabolomic analysis revealed up-regulation of lipid and lipid-like molecules, as well as flavonoid metabolism, which contribute to improved drought resistance in D. pedata under stress. Furthermore, REE addition further up-regulated flavonoid and anthocyanin synthesis compared to drought stress alone, enhancing the plant’s resilience to drought. These findings suggest that D. pedata responds to drought stress by modulating enzyme activities, osmoregulatory substances, and metabolic pathways upon REE exposure. This study underscores the dual role of REEs in enhancing both the drought tolerance and enrichment capacity of D. pedata in IARE mining areas, which is crucial for sustaining plant growth amidst drought stress, and provides new ideas for the ecological restoration and sustainable development of IARE mining areas.

Seed Priming with Zinc Oxide Nanoparticles and/or Calcium Ion: Alleviation Potential for Salt Toxicity in Tomato (Solanum lycopersicum) through Modulation of Physiochemical Attributes and Antioxidant Enzyme Activity

Seed Priming with Zinc Oxide Nanoparticles and/or Calcium Ion: Alleviation Potential for Salt Toxicity in Tomato (Solanum lycopersicum) through Modulation of Physiochemical Attributes and Antioxidant Enzyme Activity

Comprehensive assessment of phytochemicals and bioactivities in various sprouts

A comparative analysis was conducted on seventeen sprouts from vegetable and non-vegetable sources belonging to various plant families such as Asteraceae, Brassicaceae, Fabaceae, and Poaceae. The study focused on evaluating their phytochemical composition (total phenolics, glucosinolates, and anthocyanins), antioxidant capacity (DPPH assay), antidiabetic activity (inhibition of α-glucosidase and α-amylase), and hypocholesterolemic effect (inhibition of HMGR). Multivariate statistical analysis indicated that vegetable sprouts generally exhibited higher levels of phytochemicals and bioactivities compared to cereal sprouts. Red radish sprouts, in particular, showed the highest concentrations of all analyzed phytochemicals and significant bioactivities. Principal component analysis and Pearson correlation analysis underscored the importance of antioxidants, which subsequently affect antidiabetic and hypocholesterolemic activities. Among the phytochemicals, phenolic compounds and glucosinolates were highlighted as more significant than anthocyanins, considering their types and synergistic effects. Molecular docking analysis suggested that these compounds possess strong affinity and specificity towards the enzymes mentioned, indicating their potential for innovative therapeutic interventions aimed at modulating enzyme activity.

The roles of the gut microbiota, metabolites, and epigenetics in the effects of maternal exercise on offspring metabolism.

Metabolic diseases, including obesity, dyslipidemia, and type 2 diabetes, have become severe challenges worldwide. The Developmental Origins of Health and Disease (DOHaD) hypothesis suggests that an adverse intrauterine environment can increase the risk of metabolic disorders in offspring. Studies have demonstrated that maternal exercise is an effective intervention for improving the offspring metabolic health. However, the pathways through which exercise works are unclear. It has been reported that the gut microbiota mediates the effect of maternal exercise on offspring metabolism, and epigenetic modifications have also been proposed to be important molecular mechanisms. Microbial metabolites can influence epigenetics by providing substrates for DNA or histone modifications, binding to G-protein-coupled receptors to affect downstream pathways, or regulating the activity of epigenetic modifying enzymes. This review aims to summarize the intergenerational effect of maternal exercise and proposes that gut microbiota-metabolites-epigenetic regulation is an important mechanism by which maternal exercise improves offspring metabolism, which may yield novel targets for the early prevention and intervention of metabolic diseases.

Parallel phosphoproteomics and metabolomics map the global metabolic tyrosine phosphoproteome

Tyrosine phosphorylation of metabolic enzymes is an evolutionarily conserved posttranslational modification that facilitates rapid and reversible modulation of enzyme activity, localization, or function. Despite the high abundance of tyrosine phosphorylation events detected on metabolic enzymes in high-throughput mass spectrometry-based studies, functional characterization of tyrosine phosphorylation sites has been limited to a subset of enzymes. Since tyrosine phosphorylation is dysregulated across human diseases, including cancer, understanding the consequences of metabolic enzyme tyrosine phosphorylation events is critical for informing disease biology and therapeutic interventions. To globally identify metabolic enzyme tyrosine phosphorylation events and simultaneously assign functional significance to these sites, we performed parallel phosphoproteomics and polar metabolomics in nontumorigenic mammary epithelial cells (MCF10A) stimulated with epidermal growth factor (EGF) in the absence or presence of the EGF receptor inhibitor erlotinib. We performed an integrated analysis of the phosphoproteomic and metabolomic datasets to identify tyrosine phosphorylation sites on metabolic enzymes with functional consequences. We identified two previously characterized (pyruvate kinase muscle isozyme, phosphoglycerate mutase 1) and two uncharacterized (glutathione S-transferase Pi 1, glutamate dehydrogenase 1) tyrosine phosphorylation sites on metabolic enzymes with purported functions based on metabolomic analyses. We validated these hits using a doxycycline-inducible CRISPR interference system in MCF10A cells, in which target metabolic enzymes were depleted with simultaneous reexpression of wild-type, phosphomutant, or phosphomimetic isoforms. Together, these data provide a framework for identification, prioritization, and characterization of tyrosine phosphorylation sites on metabolic enzymes with functional significance.

Light-Induced Nanobody-Mediated Targeted Protein Degradation for Metabolic Flux Control.

In metabolic engineering, increasing chemical production usually involves manipulating the expression levels of key enzymes. However, limited synthetic tools exist for modulating enzyme activity beyond the transcription level. Inspired by natural post-translational mechanisms, we present targeted enzyme degradation mediated by optically controlled nanobodies. We applied this method to a branched biosynthetic pathway, deoxyviolacein, and observed enhanced product specificity and yield. We then extend the biosynthesis pathway to violacein and show how simultaneous degradation of two target enzymes can further shift production profiles. Through the redirection of metabolic flux, we demonstrate how targeted enzyme degradation can be used to minimize unwanted intermediates and boost the formation of desired products.

Sonodynamic and Acoustically Responsive Nanodrug Delivery System: Cancer Application.

The advent of acoustically responsive nanodrugs that are specifically optimized for sonodynamic therapy (SDT) is a novel approach for clinical applications. Examining the therapeutic applications of sono-responsive drug delivery systems, understanding their dynamic response to acoustic stimuli, and their crucial role in enhancing targeted drug delivery are intriguing issues for current cancer treatment. Specifically, the suggested review covers SDT, a modality that enhances the cytotoxic activity of specific compounds (sonosensitizers) using ultrasound (US). Notably, SDT offers significant advantages in cancer treatment by utilizing US energy to precisely target and activate sonosensitizers toward deep-seated malignant sites. The potential mechanisms underlying SDT involve the generation of radicals from sonosensitizers, physical disruption of cell membranes, and enhanced drug transport into cells via US-assisted sonoporation. In particular, SDT is emerging as a promising modality for noninvasive, site-directed elimination of solid tumors. Given the complexity and diversity of tumors, many studies have explored the integration of SDT with other treatments to enhance the overall efficacy. This trend has paved the way for SDT-based multimodal synergistic cancer therapies, including sonophototherapy, sonoimmunotherapy, and sonochemotherapy. Representative studies of these multimodal approaches are comprehensively presented, with a detailed discussion of their underlying mechanisms. Additionally, the application of audible sound waves in biological systems is explored, highlighting their potential to influence cellular processes and enhance therapeutic outcomes. Audible sound waves can modulate enzyme activities and affect cell behavior, providing novel avenues for the use of sound-based techniques in medical applications. This review highlights the current challenges and prospects in the development of SDT-based nanomedicines in this rapidly evolving research field. The anticipated growth of this SDT-based therapeutic approach promises to significantly improve the precision of cancer treatment.

Palmitoleic Acid Inhibits Hepatotoxic Effects by Reducing Trimethylamine-N-Oxide (TMAO) Formation in High L-Carnitine-Treated Mice.

This study investigated the effects of palmitoleic acid (POA) consumption on liver function, intestinal microbiota, and trimethylamine-N-oxide (TMAO) levels in the serum of mice treated with 3% L-carnitine drinking water. The purpose was to highlight the impact of POA on liver injury associated with high L-carnitine intake. A correlation analysis was carried out. The physiological and biochemical results showed that the administration of POA could alleviate liver injury induced by high L-carnitine ingestion, as reflected by a reduction in liver function indices (ALT, AST, AKP, and TBA activities) and modulation of antioxidant enzyme activities (SOD, GSH-Px, MDA, and RAHFR). The study also monitored the levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). Additionally, to assess the impact of POA on intestinal microbiota, we conducted a 16S rRNA high-throughput sequencing analysis. The findings indicated that POA administration resulted in lower levels of TMAO in treated mice. Furthermore, POA could regulate the composition of intestinal microbiota in L-carnitine mice, particularly affecting Bacteroides vulgatus, Parabacteroides distasonis, Alistipes shahii, Lachnospiraceae NK4A136 group, and Parasutterella secunda, which were closely related to liver injury. In summary, POA could repair liver damage caused by high intake of L-carnitine by regulating the distribution of intestinal flora and subsequently decreasing serum TMAO levels.

Research Progress on Antioxidant Peptides from Fish By-Products: Purification, Identification, and Structure-Activity Relationship.

Background/Objectives: Excessive reactive oxygen species (ROS) can lead to oxidative stress, which has become an urgent problem requiring effective solutions. Due to the drawbacks of chemically synthesized antioxidants, there is a growing interest in natural antioxidants, particularly antioxidant peptides. Methods: By reviewing recent literature on antioxidant peptides, particularly those extracted from various parts of fish, summarize which fish by-products are more conducive to the extraction of antioxidant peptides and elaborate on their characteristics. Results: This article summarizes recent advancements in extracting antioxidant peptides from fish processing by-products, Briefly introduced the purification and identification process of antioxidant peptides, specifically focusing on the extraction of antioxidant peptides from various fish by-products. Additionally, this article comprehensively reviews the relationship between amino acid residues that compose antioxidant peptides and their potential mechanisms of action. It explores the impact of amino acid types, molecular weight, and structure-activity relationships on antioxidant efficacy. Conclusions: Different amino acid residues can contribute to the antioxidant activity of peptides by scavenging free radicals, chelating metal ions, and modulating enzyme activities. The smaller the molecular weight of the antioxidant peptide, the stronger its antioxidant activity. Additionally, the antioxidant activity of peptides is influenced by specific amino acids located at the C-terminus and N-terminus positions. Simultaneously, this review provides a more systematic analysis and a broader perspective based on existing research, concluded that fish viscera are more favorable for the extraction of antioxidant peptides, providing new insights for the practical application of fish by-products. This could increase the utilization of fish viscera and reduce the environmental pollution caused by their waste, offering valuable references for the study and application of antioxidant peptides from fish by-products.

Frequency-Dependent Antioxidant Responses in HT-1080 Human Fibrosarcoma Cells Exposed to Weak Radio Frequency Fields.

This study explores the complex relationship between radio frequency (RF) exposure and cancer cells, focusing on the HT-1080 human fibrosarcoma cell line. We investigated the modulation of reactive oxygen species (ROS) and key antioxidant enzymes, including superoxide dismutase (SOD), peroxidase, and glutathione (GSH), as well as mitochondrial superoxide levels and cell viability. Exposure to RF fields in the 2-5 MHz range at very weak intensities (20 nT) over 4 days resulted in distinct, frequency-specific cellular effects. Significant increases in SOD and GSH levels were observed at 4 and 4.5 MHz, accompanied by reduced mitochondrial superoxide levels and enhanced cell viability, suggesting improved mitochondrial function. In contrast, lower frequencies like 2.5 MHz induced oxidative stress, evidenced by GSH depletion and increased mitochondrial superoxide levels. The findings demonstrate that cancer cells exhibit frequency-specific sensitivity to RF fields even at intensities significantly below current safety standards, highlighting the need to reassess exposure limits. Additionally, our analysis of the radical pair mechanism (RPM) offers deeper insight into RF-induced cellular responses. The modulation of ROS and antioxidant enzyme activities is significant for cancer treatment and has broader implications for age-related diseases, where oxidative stress is a central factor in cellular degeneration. The findings propose that RF fields may serve as a therapeutic tool to selectively modulate oxidative stress and mitochondrial function in cancer cells, with antioxidants playing a key role in mitigating potential adverse effects.

Assessment of 11 β-Hydroxysteroid Dehydrogenase Type I Activity in Patients with Psoriasis Vulgaris

Abstract Psoriasis is a chronic relapsing dermatological disease that affects around 1–3% of the world’s population and the prevalence has been increasing globally over the past years. A complex multifactorial etiology is suggested to be the underlying mechanism, involving both genetic and environmental factors that can initiate psoriatic inflammation, including mild trauma, sunburn, or chemical irritants. The interaction between these factors can disrupt the epidermal homeostasis, which triggers a viscous inflammatory circle that leads to epidermal hyperplasia and psoriasis. This inflammatory cascade is the outcome of interaction between epidermal DCs, T lymphocytes and keratinocytes. However, the initial stimulus for DCs stimulation and T cells differentiation is still unclear. In psoriasis, there is a hormonal disturbance in the form of defective GC secretion associated with HPA axis dysfunction. Recently, accumulating evidence established the presence of cutaneous steroidogenesis. The most important of this pathway is the final step controlled by 11βHSD. This enzyme by its 2 types can control local levels of activated GCs in the skin. The balance between 11βHSD1 and 11βHSD2 enzymes, which convert active cortisol/inactive cortisone, is the key to maintain skin barrier function, hence a healthy skin. This case-control study was conducted at Ain Shams University hospitals. The study was conducted on thirty-one patients with dermatologist-confirmed diagnosis of chronic plaque psoriasis and thirty age matched healthy controls. Punch biopsies were taken from lesional and non lesional sites in patients and from controls for assessment of the enzyme by ELISA, besides histopathological and immunohistochemical assessment. Our study showed that 11βHSD1 activity was significantly decreased in psoriasis patients in comparison to healthy volunteers. Besides, 11βHSD1 enzyme level was found to be decreased in lesional than non lesional skin in psoriasis patients. Further histopathological assessment revealed that the lower enzyme levels are associated with greater epidermal acanthosis and higher degree of immunostaining by anti-FGF-2, which indicates the major role of 11βHSD1 in controlling psoriatic inflammation. This was supported by the positive correlation between the non lesional enzyme level and the longest period of remission that we detected in our patients. Surprisingly, there was no significant correlation between the lesional or non lesional enzyme levels in patients with PASI score. Yet, the calculation of PASI score depends on several external factors that should be considered. Interestingly, PSS was not correlated with 11βHSD1 level in psoriasis patients but was negatively correlated with the enzyme level only in healthy controls. This supports the role of stress in modifying enzyme activity, however, in psoriasis epidermal proliferation and the presence of inflammatory infiltrate definitely affects the enzyme level. Better understanding of the complex symphony between all the players of psoriasis pathogenesis will reveal the role of 11βHSD1 and factors affecting its level in psoriasis vulgaris.

Molecular docking and dynamics simulation analysis of PDE5 inhibitor candidates for erectile dysfunction treatment.

Molecular docking studies were conducted to assess the binding affinities of five potential inhibitor candidates [PDB (Protein Data Bank) ID: 6L6E] against Phosphodiesterase 5 (PDE5), with Sildenafil used as the reference compound. The aim of this study is to reveal the potential inhibitory role of plant-derived compounds compared to Sildenafil, a PDE5 inhibitor. Autodock Vina v. 1.2.5 software was used to dock the protein and each ligand individually. Molecular dynamics simulations assessed the binding affinity of two compounds to the Phosphodiesterase 5A1 (PDE5 A1) enzyme and were carried out using GROMACS 2022.2 RESULTS: Boesenbergin A exhibited the highest affinity at -8.8 kcal/mol, followed by Ginkolide B at -8.5 kcal/mol, Sildenafil at -8.1 kcal/mol, Montanol at -7.8 kcal/mol, Beta-sitosterol at -7.1 kcal/mol, and Eugenol acetate at -6.9 kcal/mol, ranked in descending order. As a result of molecular docking studies, molecular dynamic simulations were performed for Boesenbergin A, which has the highest affinity, and Sildenafil, which is the standard molecule. Among the two ligands tested, Boesenbergin A exhibited superior binding affinity, surpassing even the standard molecule, Sildenafil. This suggests their potential for modulating enzyme activity and potential relevance in erectile dysfunction treatment.

Redistribution of SOD3 expression due to R213G polymorphism affects pulmonary interstitial macrophage reprogramming in response to hypoxia.

The extracellular isoform of superoxide dismutase (SOD3) is decreased in patients and animals with pulmonary hypertension (PH). The human R213G single-nucleotide polymorphism (SNP) in SOD3 causes its release from tissue extracellular matrix (ECM) into extracellular fluids, without modulating enzyme activity, increasing cardiovascular disease risk in humans and exacerbating chronic hypoxic PH in mice. Given the importance of interstitial macrophages (IMs) to PH pathogenesis, this study aimed to determine whether R213G SOD3 increases IM accumulation and alters IM reprogramming in response to hypoxia. R213G mice and wild-type (WT) controls were exposed to hypobaric hypoxia for 4 or 14 days compared with normoxia. Flow cytometry demonstrated a transient increase in IMs at day 4 in both strains. Contrary to our hypothesis, the R213G SNP did not augment IM accumulation. To determine strain differences in the IM reprogramming response to hypoxia, we performed RNAsequencing on IMs isolated at each timepoint. We found that IMs from R213G mice exposed to hypoxia activated ECM-related pathways and a combination of alternative macrophage and proinflammatory signaling. Furthermore, when compared with WT responses, IMs from R213G mice lacked metabolic remodeling and demonstrated a blunted anti-inflammatory response between the early (day 4) and later (day 14) timepoints. We confirmed metabolic responses using Agilent Seahorse assays, whereby WT, but not R213G, IMs upregulated glycolysis at day 4 that returned to baseline at day 14. Finally, we identify differential regulation of several redox-sensitive upstream regulators that could be investigated in future studies.NEW & NOTEWORTHY Redistributed expression of SOD3 out of tissue ECM due to the human R213G SNP exacerbates chronic hypoxic PH. Highlighting the importance of macrophage phenotype, our findings reveal that the R213G SNP does not exacerbate pulmonary macrophage accumulation in response to hypoxia but influences their metabolic and phenotypic reprogramming. We demonstrate a deficiency in the metabolic response to hypoxic stress in R213G macrophages, associated with weakened inflammatory resolution and activation of profibrotic pathways implicated in PH.

Effect of magnetic field treatment on the softening of green chilies (Capsicum annuum L.) during storage

In this study, effects of magnetic field treatment on the softening of green chilies during storage (0–30 d at 10 °C) were investigated, and the cell wall polysaccharide content, modifying enzyme activities, water distribution, and cell wall structure were determined. After 30 d of storage, the weight loss of the green chilies in conventional refrigeration (CR) group reached 35.40 %, whereas it was 20.96 % and 29.85 % in the static (SMF; 4 mT) and alternating magnetic field (AMF; 4 mT, 1 Hz) groups, respectively. Furthermore, magnetic field treatment maintained low levels of water-soluble pectin (WSP) and high levels of chelate-soluble pectin (CSP) and sodium carbonate-soluble pectin (NSP) in the green chilies. The degree of methylation (DE) values of WSP and NSP in the pre-treated samples were 0.37 and 0.18, respectively. Conversely, at the end of storage, the DE values of WSP and NSP in the CR, SMF, and AMF groups decreased to 0.12 and 0.05, 0.25 and 0.11, and 0.18 and 0.07, respectively, suggesting that magnetic field treatment had a negative influence on the demethylation of pectin. Magnetic field treatment also decreased the activities of pectin methyl esterase, polygalacturonase, and β-galactosidase in the green chilies, maintaining them at a low level. The magnetic field treatment resulted in a higher free water content in green chilies compared to the CR, exceeding the CR group’s content by 1.79 % and reaching 88.18 % at the terminal storage. Scanning electron microscopy results revealed that magnetic field treatment maintained the structural integrity of the cell wall in the green chilies. The results of this study confirmed the applicability of magnetic field treatment in maintaining the firmness and reducing the weight loss of the green chilies, thus prolonging their shelf life.

Mycorrhizal and non-mycorrhizal perennial ryegrass roots exhibit differential regulation of lipid and Ca2+ signaling pathways in response to low and high temperature stresses

Lipids and Ca2+ are involved as intermediate messengers in temperature-sensing signaling pathways. Arbuscular mycorrhizal (AM) symbiosis is a mutualistic symbiosis between fungi and terrestrial plants that helps host plants cope with adverse environmental conditions. Nonetheless, the regulatory mechanisms of lipid- and Ca2+-mediated signaling pathways in mycorrhizal plants under cold and heat stress have not been determined. The present work focused on investigating the lipid- and Ca2+-mediated signaling pathways in arbuscular mycorrhizal (AM) and non-mycorrhizal (NM) roots under temperature stress and determining the role of Ca2+ levels in AM symbiosis and temperature stress tolerance in perennial ryegrass (Lolium perenne L.) Compared with NM plants, AM symbiosis increased phosphatidic acid (PA) and Ca2+ signaling in the roots of perennial ryegrass, increasing the expression of genes associated with low temperature (LT) stress, including LpICE1, LpCBF3, LpCOR27, LpCOR47, LpIRI, and LpAFP, and high temperature (HT) stress, including LpHSFC1b, LpHSFC2b, LpsHSP17.8, LpHSP22, LpHSP70, and LpHSP90, under LT and HT conditions. These effects result in modulated antioxidant enzyme activities, reduced lipid peroxidation, and suppressed growth inhibition caused by LT and HT stresses. Furthermore, exogenous Ca2+ application enhanced AM symbiosis, leading to the upregulation of Ca2+ signaling pathway genes in roots and ultimately promoting the growth of perennial ryegrass under LT and HT stresses. These findings shed light on lipid and Ca2+ signal transduction in AM-associated plants under LT and HT stresses, emphasizing that Ca2+ enhances cold and heat tolerance in mycorrhizal plants.

Aromatic residues in N-terminal domain of archaeal trehalase affect the folding and activity of catalytic domain

Considering the structure of the bacterial GH15 family glucoamylase (GA), Thermoplasma trehalase Tvn1315 may be composed of a β-sandwich domain (BD) and a catalytic domain (CD). Tvn1315 BD weakly binds to insoluble β-glucans, such as cellulose, and helps fold CD. To determine how aromatic residues contribute to proper folding and enzyme activity, we performed alanine scanning for 32 aromatic residues in the BD. The study did not identify a single residue involved in glucan binding. However, several aromatic residues were found to be involved in BD or CD folding and in modulating the activity of the full-length enzyme. Among those aromatic residue mutations, the W43A mutation led to reduced solubility of the BD and full-length protein and resulted in a full-length enzyme with significantly lower activity. The activity of W43F and W43Y was significantly higher than that of W43A. In addition, Ala substitutions of Tyr83, Tyr113, and Tyr17 led to a reduction in trehalase activity, but Phe substitutions of these residues could be tolerated, as these mutants maintained activities similar to WT activity. Thus, these aromatic residues in BD may interact with CD and modulate enzyme activity.Key points• Aromatic residues in the BD are involved in BD and CD folding.• Aromatic residues in the BD near the CD active site modulate enzyme activity.• BD interacts with CD and closely modulates enzyme activity.