ABSTRACT
After viral infection, the virus relies on the host cell's complex metabolic and biosynthetic machinery for replication. However, the impact of avian influenza virus (AIV) on metabolites and gene expression in poultry cells remains unclear. To investigate this, we infected chicken embryo fibroblasts DF1 cells with H9N2 AIV at an MOI of 3. Our aim was to explore how H9N2 AIV alters DF1 cells metabolic pathways to facilitate its replication. We employed metabolomics and transcriptomics techniques to analyze changes in metabolite content and gene expression. Metabolomics analysis revealed a significant increase in glutathione-related metabolites, including reduced glutathione (GSH), oxidized glutathione (GSSG) and total glutathione (T-GSH) upon H9N2 AIV infection in DF1 cells. Elisa results confirmed elevated levels of GSH, GSSG, and T-GSH consistent with metabolomics findings, noting a pronounced increase in GSSG compared to GSH. Transcriptomics showed significant alterations in genes involved in glutathione synthesis and metabolism post-H9N2 infection. However, adding the glutathione synthesis inhibitor BSO exogenously significantly promoted H9N2 replication in DF1 cells. This was accompanied by increased mRNA levels of pro-inflammatory cytokines (IL-1ß, IFN-γ) and decreased mRNA levels of anti-inflammatory cytokines (TGF-ß, IL-13). BSO also reduced catalase (CAT) gene expression and inhibited its activity, leading to higher reactive oxygen species (ROS) and malondialdehyde (MDA) level in DF1 cells. qPCR results indicated decreased mRNA levels of Nrf2, NQO1, and HO-1 with BSO, ultimately increasing oxidative stress in DF1 cells. Therefore, the above results indicated that H9N2 AIV infection in DF1 cells activated the glutathione metabolic pathway to enhance the cell's self-defense mechanism against H9N2 replication. However, when GSH synthesis is inhibited within the cells, it leads to an elevated oxidative stress level, thereby promoting H9N2 replication within the cells through Nrf2/HO-1 pathway. This study provides a theoretical basis for future rational utilization of the glutathione metabolic pathway to prevent viral replication.
ABSTRACT
Migraine as a common neurological disorder still lacks effective therapies. Tetramethylpyrazine (TMP) is the main bioactive component from Ligusticum chuanxiong hort., a traditional edible-medicinal herb. This study aimed to investigate the action of TMP on migraine by metabolomics with mass spectrometry imaging (MSI) analysis and molecular exploring, including random forest model analysis, KEGG enrichment analysis and metabolite-metabolite interaction network analysis. The results indicated that 26 key representative metabolic biomarkers were identified, especially γ-glu-cys, which were highly related to glutathione (GSH) metabolism. MSI found the abundance of eleven endogenous metabolites were modulated by TMP, particularly glucose, the most important energy metabolism molecule, and GSH were increased that maintains intracellular redox balance, which was consistent with activation of Nrf2 signals by TMP. These findings provide insights into the effectiveness of metabolomics integrated with MSI in explaining the metabolic mechanisms of TMP, and afford valuable information for healthy development of TMP in migraine.
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BACKGROUND: Pruning is an important cultivation management option that has important effects on peach yield and quality. However, the effects of pruning on the overall genetic and metabolic changes in peach leaves and fruits are poorly understood. RESULTS: The transcriptomic and metabolomic profiles of leaves and fruits from trees subjected to pruning and unpruning treatments were measured. A total of 20,633 genes and 622 metabolites were detected. Compared with those in the control, 1,127 differentially expressed genes (DEGs) and 77 differentially expressed metabolites (DEMs) were identified in leaves from pruned and unpruned trees (pdLvsupdL), whereas 423 DEGs and 29 DEMs were identified in fruits from the pairwise comparison pdFvsupdF. The content of three auxin analogues was upregulated in the leaves of pruned trees, the content of all flavonoids detected in the leaves decreased, and the expression of almost all genes involved in the flavonoid biosynthesis pathway decreased. The phenolic acid and amino acid metabolites detected in fruits from pruned trees were downregulated, and all terpenoids were upregulated. The correlation analysis revealed that DEGs and DEMs in leaves were enriched in tryptophan metabolism, auxin signal transduction, and flavonoid biosynthesis. DEGs and DEMs in fruits were enriched in flavonoid and phenylpropanoid biosynthesis, as well as L-glutamic acid biosynthesis. CONCLUSIONS: Pruning has different effects on the leaves and fruits of peach trees, affecting mainly the secondary metabolism and hormone signalling pathways in leaves and amino acid biosynthesis in fruits.
Subject(s)
Fruit , Gene Expression Profiling , Metabolomics , Plant Leaves , Prunus persica , Plant Leaves/metabolism , Plant Leaves/genetics , Prunus persica/genetics , Prunus persica/metabolism , Prunus persica/growth & development , Fruit/metabolism , Fruit/genetics , Fruit/growth & development , Gene Expression Regulation, Plant , Metabolome , Transcriptome , Flavonoids/metabolism , Indoleacetic Acids/metabolismABSTRACT
Low temperature is the most common abiotic factor that usually occurs during the seed germination of alfalfa (Medicago sativa L.). However, the potential regulatory mechanisms involved in alfalfa seed germination under low temperature stress are still ambiguous. Therefore, to determine the relevant key genes and pathways, the phenotypic and transcriptomic analyses of low-temperature sensitive (Instict) and low-temperature tolerant (Sardi10) alfalfa were conducted at 6 and 15 h of seed germination under normal (20 °C) and low (10 °C) temperature conditions. Germination phenotypic results showed that Sardi10 had the strongest germination ability under low temperatures, which was manifested by the higher germination-related indicators. Further transcriptome analysis indicated that differentially expressed genes were mainly enriched in galactose metabolism and carbon metabolism pathways, which were the most commonly enriched in two alfalfa genotypes. Additionally, fatty acid metabolism and glutathione metabolism pathways were preferably enriched in Sardi10 alfalfa. The Weighted Gene Co-Expression Network Analysis (WGCNA) suggested that genes were closely related to galactose metabolism, fatty acid metabolism, and glutathione metabolism in Sardi10 alfalfa at the module with the highest correlation (6 h of germination under low temperature). Finally, qRT-PCR analysis further validated the related genes involved in the above pathways, which might play crucial roles in regulating seed germination of alfalfa under low temperature conditions. These findings provide new insights into the molecular mechanisms of seed germination underlying the low temperature stress in alfalfa.
Subject(s)
Gene Expression Profiling , Gene Expression Regulation, Plant , Germination , Medicago sativa , Phenotype , Seeds , Transcriptome , Medicago sativa/genetics , Medicago sativa/physiology , Medicago sativa/metabolism , Germination/genetics , Seeds/genetics , Seeds/growth & development , Gene Expression Profiling/methods , Cold Temperature , Cold-Shock Response/genetics , Gene Regulatory NetworksABSTRACT
Ferroptosis, an iron-dependent form of regulated cell death, has received increasing attention for its pathophysiologic contribution to the onset and development of doxorubicin-induced cardiotoxicity. Moreover, modulation of ferroptosis with specific inhibitors may provide new therapeutic opportunities for doxorubicin-induced cardiotoxicity. Here, we will review the molecular mechanisms and therapeutic promise of targeting ferroptosis in doxorubicin-induced cardiotoxicity.
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Introduction: Arbuscular mycorrhizal fungi (AMF) and dark septate endophytic fungi (DSEs) generally coexist in the roots of plants. However, our understanding of the effects of their coexistence on plant growth and stress resistance is limited. Methods: In the present study, the effects of single and dual inoculation of AMF and DSE on the growth, photosynthetic physiology, glutathione (GSH) metabolism, endogenous hormones, and cadmium (Cd) content of maize under 25 mgâ¢kg-1 Cd stress were investigated. Results: Compared with that after the non-inoculation treatment, AMF+DSE co-inoculation significantly increased the photosynthetic rate (Pn) of maize leaves; promoted root GSH metabolism; increased the root GSH concentration and activity of γ-glutamyl cysteine synthase (γ-GCS), ATP sulfatase (ATPS) and sulfite reductase (SIR) by 215%, 117%, 50%, and 36%, respectively; and increased the concentration of endogenous hormones in roots, with increases in zeatin (ZR), indole-3 acetic acid (IAA), and abscisic acid (ABA) by 81%, 209%, and 72%, respectively. AMF inoculation, DSE inoculation and AMF+DSE co-inoculation significantly increased maize biomass, and single inoculation with AMF or DSE increased the Cd concentration in roots by 104% or 120%, respectively. Moreover, significant or highly significant positive correlations were observed between the contents of ZR, IAA, and ABA and the activities of γ-GCS, ATPS, and SIR and the glutathione (GSH) content. There were significant or highly significant positive interactions between AMF and DSE on the Pn of leaves, root GSH metabolism, and endogenous hormone contents according to two-way analysis of variance. Therefore, the coexistence of AMF and DSE synergistically enhanced the Cd tolerance of maize.
ABSTRACT
Lowing blood lipid levels with probiotics has good application prospects. This study aimed to isolate probiotics with hypolipidemic efficacy from homemade na dish and investigate their mechanism of action. In vitro experiments were conducted to determine the cholesterol-lowering ability of five isolates, with results showing that Lactiplantibacillus plantarum N4 exhibited a high cholesterol-lowering rate of 50.27% and significant resistance to acid (87%), bile salt (51.97%), and pepsin (88.28%) in simulated gastrointestinal fluids, indicating promising application prospects for the use of probiotics in lowering blood lipids. The findings from the in vivo experiment demonstrated that the administration of N4 effectively attenuated lipid droplet accumulation and inflammatory cell infiltration in the body weight and liver of hyperlipidemic rats, leading to restoration of liver tissue morphology and structure, as well as improvement in lipid and liver biochemical parameters. 16S analysis indicated that the oral administration of N4 led to significant alterations in the relative abundance of various genera, including Sutterella, Bacteroides, Clostridium, and Ruminococcus, in the gut microbiota of hyperlipidemia rats. Additionally, fecal metabolomic analysis identified a total of 78 metabolites following N4 intervention, with carboxylic acids and their derivatives being the predominant compounds detected. The transcriptomic analysis revealed 156 genes with differential expression following N4 intervention, leading to the identification of 171 metabolic pathways through Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Notably, the glutathione metabolism pathway, PPAR signaling pathway, and bile secretion pathway emerged as the primary enrichment pathways. The findings from a comprehensive multi-omics analysis indicate that N4 influences lipid metabolism and diminishes lipid levels in hyperlipidemic rats through modulation of fumaric acid and γ-aminobutyric acid concentrations, as well as glutathione and other metabolic pathways in the intestinal tract, derived from both the gut microbiota and the host liver. This research offers valuable insights into the therapeutic potential of probiotics for managing lipid metabolism disorders and their utilization in the development of functional foods.
ABSTRACT
Cancer cells can induce molecular changes that reshape cellular metabolism, creating specific vulnerabilities for targeted therapeutic interventions. Given the importance of reactive oxygen species (ROS) in tumor development and drug resistance, and the abundance of reduced glutathione (GSH) as the primary cellular antioxidant, we examined an integrated panel of 56 glutathione metabolism-related genes (GMRGs) across diverse cancer types. This analysis revealed a remarkable association between GMRGs and low-grade glioma (LGG) survival. Unsupervised clustering and a GMRGs-based risk score (GS) categorized LGG patients into two groups, linking elevated glutathione metabolism to poorer prognosis and treatment outcomes. Our GS model outperformed established clinical prognostic factors, acting as an independent prognostic factor. GS also exhibited correlations with pro-tumor M2 macrophage infiltration, upregulated immunosuppressive genes, and diminished responses to various cancer therapies. Experimental validation in glioma cell lines confirmed the critical role of glutathione metabolism in glioma cell proliferation and chemoresistance. Our findings highlight the presence of a unique metabolic susceptibility in LGG and introduce a novel GS system as a highly effective tool for predicting the prognosis of LGG.
Subject(s)
Brain Neoplasms , Glioma , Glutathione , Glioma/genetics , Glioma/metabolism , Glioma/pathology , Glioma/therapy , Glutathione/metabolism , Humans , Prognosis , Brain Neoplasms/genetics , Brain Neoplasms/metabolism , Brain Neoplasms/pathology , Cell Line, Tumor , Gene Expression Regulation, Neoplastic , Neoplasm Grading , Cell Proliferation/genetics , Female , Drug Resistance, Neoplasm/genetics , Treatment OutcomeABSTRACT
Familial adenomatous polyposis (FAP) patients face an almost certain 100% risk of developing colorectal cancer, necessitating prophylactic colectomy to prevent disease progression. A crucial goal is to hinder this progression. In a recent clinical trial involving 14 FAP patients, half received 60 g of black raspberry (BRB) powder orally and BRB suppositories at bedtime, while the other half received only BRB suppositories at bedtime over 9 months. This intervention led to a notable reduction in rectal polyps for 11 patients, although 3 showed no response. In this study, we delved into the metabolic changes induced by BRBs in the same patient cohort. Employing mass spectrometry-based non-targeted metabolomics, we analyzed pre- and post-BRB urinary and plasma samples from the 11 responders. The results showed significant alterations in 23 urinary and 6 plasma metabolites, influencing various pathways including polyamine, glutathione metabolism, the tricarboxylic acid cycle, inositol metabolism, and benzoate production. BRBs notably elevated levels of several metabolites associated with these pathways, suggesting a potential mechanism through which BRBs facilitate rectal polyp regression in FAP patients by modulating multiple metabolic pathways. Notably, metabolites derived from BRB polyphenols were significantly increased post-BRB intervention, emphasizing the potential therapeutic value of BRBs in FAP management.
ABSTRACT
Alcoholic liver disease (ALD) is a serious health threat. Soybean meal peptide (SMP) supplementation may protect against this damage; however, the potential mechanism underlying the specific sequence of SMPs is unclear. Protein-protein interaction and proteomic analyses are effective methods for studying functional ingredients in diseases. This study aimed to investigate the potential mechanism of action of the peptide Gly-Thr-Tyr-Trp (GTYW) on ALD using protein-protein interaction and proteomic analyses. These results demonstrate that GTYW influenced the targets of glutathione metabolism (glutathione-disulfide reductase, glutathione S-transferase pi 1, and glutathione S-transferase mu 2). It also regulated the expression of targets related to energy metabolism and amino acid conversion (trypsin-2, cysteine dioxygenase type-1, and F6SJM7). Amino acid and lipid metabolisms were identified based on Gene Ontology annotation. These results indicate that GTYW might affect alcohol-related liver disease signaling pathways. This study provides evidence of the protective and nutritional benefits of SMPs in ALD treatment.
Subject(s)
Glycine max , Liver Diseases, Alcoholic , Peptides , Proteomics , Animals , Mice , Glycine max/chemistry , Glycine max/metabolism , Liver Diseases, Alcoholic/metabolism , Liver Diseases, Alcoholic/prevention & control , Liver Diseases, Alcoholic/genetics , Male , Peptides/chemistry , Peptides/pharmacology , Peptides/metabolism , Peptides/administration & dosage , Humans , Mice, Inbred C57BL , Protective Agents/pharmacology , Protective Agents/administration & dosage , Protective Agents/chemistry , Liver/metabolismABSTRACT
Glutathione metabolism (GM) is a crucial part of various metabolic and pathophysiological processes. However, its role in lung adenocarcinoma (LUAD) has not been comprehensively studied. This study aimed to explore the potential relationship between GM genes, the prognosis, and the immune microenvironment of patients with LUAD. We constructed a risk signature model containing seven GM genes using Lasso combined Cox regression and validated it using six GEO datasets. Our analysis showed that it is an independent prognostic factor. Functional enrichment analysis revealed that the GM genes were significantly enriched in cell proliferation, cell cycle regulation, and metabolic pathways. Clinical and gene expression data of patients with LUAD were obtained from the TCGA database and patients were divided into high- and low-risk groups. The high-risk patient group had a poor prognosis, reduced immune cell infiltration, poor response to immunotherapy, high sensitivity to chemotherapy, and low sensitivity to targeted therapy. Subsequently, single-cell transcriptome analysis using the GSE143423 and GSE127465 datasets revealed that the core SMS gene was highly enriched in M2 Macrophages. Finally, nine GEO datasets and multiple fluorescence staining revealed a correlation between the SMS expression and M2 macrophage polarization. Our prognostic model in which the core SMS gene is closely related to M2 macrophage polarization is expected to become a novel target and strategy for tumor therapy.
Subject(s)
Adenocarcinoma of Lung , Gene Expression Regulation, Neoplastic , Glutathione , Lung Neoplasms , Macrophages , Tumor Microenvironment , Humans , Adenocarcinoma of Lung/genetics , Adenocarcinoma of Lung/immunology , Adenocarcinoma of Lung/mortality , Lung Neoplasms/genetics , Lung Neoplasms/immunology , Lung Neoplasms/mortality , Prognosis , Glutathione/metabolism , Macrophages/immunology , Macrophages/metabolism , Tumor Microenvironment/immunology , Tumor Microenvironment/genetics , Databases, Genetic , Macrophage Activation/genetics , Gene Expression Profiling , Biomarkers, Tumor/genetics , FemaleABSTRACT
Spartina alterniflora is an exo-recretohalophyte Poaceae species that is able to grow well in seashore, but the genomic basis underlying its adaptation to salt tolerance remains unknown. Here, we report a high-quality, chromosome-level genome assembly of S. alterniflora constructed through PacBio HiFi sequencing, combined with high-throughput chromosome conformation capture (Hi-C) technology and Illumina-based transcriptomic analyses. The final 1.58 Gb genome assembly has a contig N50 size of 46.74 Mb. Phylogenetic analysis suggests that S. alterniflora diverged from Zoysia japonica approximately 21.72 million years ago (MYA). Moreover, whole-genome duplication (WGD) events in S. alterniflora appear to have expanded gene families and transcription factors relevant to salt tolerance and adaptation to saline environments. Comparative genomics analyses identified numerous species-specific genes, significantly expanded genes and positively selected genes that are enriched for 'ion transport' and 'response to salt stress'. RNA-seq analysis identified several ion transporter genes including the high-affinity K+ transporters (HKTs), SaHKT1;2, SaHKT1;3 and SaHKT1;8, and high copy number of Salt Overly Sensitive (SOS) up-regulated under high salt conditions, and the overexpression of SaHKT2;4 in Arabidopsis thaliana conferred salt tolerance to the plant, suggesting specialized roles for S. alterniflora to adapt to saline environments. Integrated metabolomics and transcriptomics analyses revealed that salt stress activate glutathione metabolism, with differential expressions of several genes such as γ-ECS, GSH-S, GPX, GST and PCS in the glutathione metabolism. This study suggests several adaptive mechanisms that could contribute our understanding of evolutional basis of the halophyte.
Subject(s)
Genome, Plant , Phylogeny , Poaceae , Salt Tolerance , Salt Tolerance/genetics , Genome, Plant/genetics , Poaceae/genetics , Poaceae/metabolism , Salt-Tolerant Plants/genetics , Salt-Tolerant Plants/metabolism , Gene Expression Regulation, PlantABSTRACT
BACKGROUND: Bacterial wilt caused by Ralstonia solanacearum severely affects peanut (Arachis hypogaea L.) yields. The breeding of resistant cultivars is an efficient means of controlling plant diseases. Therefore, identification of resistance genes effective against bacterial wilt is a matter of urgency. The lack of a reference genome for a resistant genotype severely hinders the process of identification of resistance genes in peanut. In addition, limited information is available on disease resistance-related pathways in peanut. RESULTS: Full-length transcriptome data were used to generate wilt-resistant and -susceptible transcript pools. In total, 253,869 transcripts were retained to form a reference transcriptome for RNA-sequencing data analysis. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of differentially expressed genes revealed the plant-pathogen interaction pathway to be the main resistance-related pathway for peanut to prevent bacterial invasion and calcium plays an important role in this pathway. Glutathione metabolism was enriched in wilt-susceptible genotypes, which would promote glutathione synthesis in the early stages of pathogen invasion. Based on our previous quantitative trait locus (QTL) mapping results, the genes arahy.V6I7WA and arahy.MXY2PU, which encode nucleotide-binding site-leucine-rich repeat receptor proteins, were indicated to be associated with resistance to bacterial wilt. CONCLUSIONS: This study identified several pathways associated with resistance to bacterial wilt and identified candidate genes for bacterial wilt resistance in a major QTL region. These findings lay a foundation for investigation of the mechanism of resistance to bacterial wilt in peanut.
Subject(s)
Arachis , Ralstonia solanacearum , Arachis/genetics , Arachis/microbiology , Transcriptome , Ralstonia solanacearum/physiology , Plant Breeding , Disease Resistance/genetics , Glutathione/genetics , Plant Diseases/genetics , Plant Diseases/microbiologyABSTRACT
BACKGROUND: Redox control seems to be indispensable for proper embryonic development. The ratio between glutathione (GSH) and its oxidized disulfide (GSSG) is the most abundant cellular redox circuit. METHODS: We used zebrafish harboring the glutaredoxin 1-redox sensitive green fluorescent protein (Grx1-roGFP) probe either in mitochondria or cytosol to test the hypothesis that the GSH:GSSG ratio is strictly regulated through zebrafish embryogenesis to sustain the different developmental processes of the embryo. RESULTS: Following the GSSG:GSH ratio as a proxy for the GSH-dependent reduction potential (EhGSH) revealed increasing mitochondrial and cytosolic EhGSH during cleavage and gastrulation. During organogenesis, cytosolic EhGSH decreased, while that of mitochondria remained high. The similarity between EhGSH in brain and muscle suggests a central regulation. Modulation of GSH metabolism had only modest effects on the GSSG:GSH ratios of newly hatched larvae. However, inhibition of GSH reductase directly after fertilization led to dead embryos already 10 h later. Exposure to the emerging environmental pollutant Perfluorooctane Sulfonate (PFOS) disturbed the apparent regulated EhGSH as well. CONCLUSIONS: Mitochondrial and cytosolic GSSG:GSH ratios are almost identical in different organs during zebrafish development indicating that the EhGSH might follow H2O2 levels and rather indirectly affect specific enzymatic activities needed for proper embryogenesis. GENERAL SIGNIFICANCE: Our data confirm that vertebrate embryogenesis depends on strictly regulated redox homeostasis. Disturbance of the GSSG:GSH circuit, e.g. induced by environmental pollution, leads to malformation and death.
Subject(s)
Cytosol , Glutathione , Mitochondria , Oxidation-Reduction , Zebrafish , Animals , Zebrafish/metabolism , Zebrafish/embryology , Glutathione/metabolism , Mitochondria/metabolism , Cytosol/metabolism , Embryonic Development , Glutathione Disulfide/metabolism , Embryo, Nonmammalian/metabolismABSTRACT
Biofortification aims to increase selenium (Se) concentration and bioavailability in edible parts of crops such as wheat (Triticum aestivum L.), resulting in increased concentration of Se in plants and/or soil. Higher Se concentrations can disturb protein structure and consequently influence glutathione (GSH) metabolism in plants which can affect antioxidative and other detoxification pathways. The aim of this study was to elucidate the impact of five different concentrations of selenate and selenite (0.4, 4, 20, 40 and 400 mg kg-1) on the ascorbate-glutathione cycle in wheat shoots and roots and to determine biochemical and molecular tissue-specific responses. Content of investigated metabolites, activities of detoxification enzymes and expression of their genes depended both on the chemical form and concentration of the applied Se, as well as on the type of plant tissue. The most pronounced changes in the expression level of genes involved in GSH metabolism were visible in wheat shoots at the highest concentrations of both forms of Se. Obtained results can serve as a basis for further research on Se toxicity and detoxification mechanisms in wheat. New insights into the Se impact on GSH metabolism could contribute to the further development of biofortification strategies.
Subject(s)
Selenium , Selenium/pharmacology , Selenium/metabolism , Triticum/metabolism , Seedlings/metabolism , Selenic Acid/metabolism , Selenious Acid/metabolism , Glutathione/metabolismABSTRACT
The interaction between plant hosts and plant viruses is a very unique and complex process, relying on dynamically modulated intercellular redox states and the generation of reactive oxygen species (ROS). Plants strive to precisely control this state during biotic stress, as optimal redox levels enable proper induction of defense mechanisms against plant viruses. One of the crucial elements of ROS regulation and redox state is the production of metabolites, such as glutathione, or the activation of glutathione-associated enzymes. Both of these elements play a role in limiting the degree of potential oxidative damage in plant cells. While the role of glutathione and specific enzymes is well understood in other types of abiotic and biotic stresses, particularly those associated with bacteria or fungi, recent advances in research have highlighted the significance of glutathione modulation and mutations in genes encoding glutathione-associated enzymes in triggering immunity or susceptibility against plant viruses. Apparently, glutathione-associated genes are involved in precisely controlling and protecting host cells from damage caused by ROS during viral infections, playing a crucial role in the host's response. In this review, we aim to outline the significant improvements made in research on plant viruses and glutathione, specifically in the context of their involvement in susceptible and resistant responses, as well as changes in the localization of glutathione. Analyses of essential glutathione-associated enzymes in susceptible and resistant responses have demonstrated that the levels of enzymatic activity or the absence of specific enzymes can impact the spread of the virus and activate host-induced defense mechanisms. This contributes to the complex network of the plant immune system. Although investigations of glutathione during the plant-virus interplay remain a challenge, the use of novel tools and approaches to explore its role will significantly contribute to our knowledge in the field.
ABSTRACT
BACKGROUND: Agaricus bisporus is a globally important edible fungus. The occurrence of ginger blotch caused by Pseudomonas 'gingeri' during A. bisporus growth and post-harvest stages results in significant economic losses. The biotoxin monoacetylphloroglucinol (MAPG) produced by P. 'gingeri' is responsible for inducing ginger blotch on A. bisporus. However, the understanding of the toxic mechanisms of MAPG on A. bisporus remains limited, which hinders the precise control of ginger blotch disease in A. bisporus and the breeding of disease-resistant varieties. RESULTS: Integrating transcriptomic, metabolomic, and physiological data revealed that MAPG led to an increase in intracellular superoxide anion (O2 -) levels and lipid peroxidation in A. bisporus. MAPG changed the cellular membrane composition of A. bisporus, causing to damage membrane permeability. MAPG inhibited the expression of genes associated with the 19s subunit of the proteasome, thereby impeding cellular waste degradation in A. bisporus. Unlike melanin, MAPG stimulated the synthesis of flavonoids in A. bisporus, which might explain the manifestation of ginger-colored symptoms rather than browning. Meanwhile, the glutathione metabolism pathway in A. bisporus played a pivotal role in counteracting the cytotoxic effects of MAPG. Additionally, enhanced catalase activity and up-regulation of defense-related genes, including cytochrome P450s, Major Facilitator Superfamily (MFS), and ABC transporters, were observed. CONCLUSION: This study provides comprehensive insights into MAPG toxicity in A. bisporus and uncovers the detoxification strategies of A. bisporus against MAPG. The findings offer valuable evidence for precise control and breeding of resistant varieties against ginger blotch in A. bisporus. © 2024 Society of Chemical Industry.
Subject(s)
Agaricus , Phloroglucinol , Plant Diseases , Pseudomonas , Plant Diseases/microbiology , Phloroglucinol/analogs & derivatives , Phloroglucinol/pharmacology , Phloroglucinol/metabolismABSTRACT
The presence of high chromium (Cr) levels induces the buildup of reactive oxygen species (ROS), resulting in hindered plant development. Riboflavin (vitamin B2) is produced by plants, fungi, and microbes. It serves as a precursor to the coenzymes flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), which play a crucial role in cellular metabolism. The objective of this work was to clarify the underlying mechanisms by which riboflavin alleviates Cr stress in Praecitrullus fistulosus L. Further, the role of riboflavin in growth, ions homeostasis, methylglyoxal detoxification, and antioxidant defense mechanism are not well documented in plants under Cr toxicity. We found greater biomass and minimal production of ROS in plants pretreated with riboflavin under Cr stress. Results manifested a clear abridge in growth, chlorophyll content, and nutrient uptake in Indian squash plants exposed to Cr stress. Findings displayed that Cr stress visibly enhanced oxidative injury reflected as higher malondialdehyde (MDA), hydrogen peroxide (H2O2), superoxide radical (O2â¢â), methylglyoxal (MG) levels alongside vivid lipoxygenase activity. Riboflavin strengthened antioxidant system, enhanced osmolyte production and improved membrane integrity. Riboflavin diminished Cr accumulation in aerial parts that led to improved nutrient acquisition. Taken together, riboflavin abridged Cr phytotoxic effects by improving redox balance because plants treated with riboflavin had strong antioxidant system that carried out effective ROS detoxification. Riboflavin protected membrane integrity that, in turn, improved nutrient uptake in plants.
Subject(s)
Antioxidants , Cucurbita , Antioxidants/metabolism , Chromium/toxicity , Chromium/metabolism , Pyruvaldehyde , Reactive Oxygen Species/metabolism , Hydrogen Peroxide/metabolism , Oxidation-Reduction , Plants/metabolism , Riboflavin/metabolismABSTRACT
BACKGROUND: Cognitive impairment (CI) is a significant public health concern, and bioactive peptides have shown potential as therapeutic agents. However, information about their synergistic effects on cognitive function is still limited. Here, we investigated the synergistic effects of tilapia head protein hydrolysate (THPH) and walnut protein hydrolysate (WPH) in mitigating CI induced by scopolamine in mice. RESULTS: The results showed that the combined supplementation of THPH and WPH (mass ratio, 1:1) was superior to either individual supplement in enhancing spatial memory and object recognition abilities in CI mice, and significantly lessened brain injury in CI mice by alleviating neuronal damage, reducing oxidative stress and stabilizing the cholinergic system. In addition, the combined supplementation was found to be more conducive to remodeling the gut microbiota structure in CI mice by not only remarkably reducing the ratio of Firmicutes to Bacteroidota, but also specifically enriching the genus Roseburia. On the other hand, the combined supplementation regulated the disorders of sphingolipid and amino acid metabolism in CI mice, particularly upregulating glutathione and histidine metabolism, and displayed a stronger ability to increase the expression of genes and proteins related to the brain-derived neurotrophic factor (BDNF)/TrkB/CrEB signaling pathway in the brain. CONCLUSION: These findings demonstrate that tilapia head and walnut-derived protein hydrolysates exerted synergistic effects in ameliorating CI, which was achieved through modulation of gut microbiota, serum metabolic pathways and BDNF signaling pathways. © 2024 Society of Chemical Industry.
Subject(s)
Brain-Derived Neurotrophic Factor , Cognitive Dysfunction , Gastrointestinal Microbiome , Juglans , Protein Hydrolysates , Tilapia , Animals , Juglans/chemistry , Protein Hydrolysates/chemistry , Protein Hydrolysates/administration & dosage , Protein Hydrolysates/pharmacology , Tilapia/metabolism , Mice , Cognitive Dysfunction/drug therapy , Cognitive Dysfunction/metabolism , Male , Brain-Derived Neurotrophic Factor/metabolism , Brain-Derived Neurotrophic Factor/genetics , Gastrointestinal Microbiome/drug effects , Fish Proteins/metabolism , Fish Proteins/chemistry , Humans , Oxidative Stress/drug effects , Plant Proteins , Drug Synergism , Cognition/drug effects , Brain/metabolism , Brain/drug effects , Dietary Supplements/analysisABSTRACT
BACKGROUND: In paddy fields, the noxious weed barnyard grass secretes 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA) to interfere with rice growth. Rice is unable to synthesize DIMBOA. Rice cultivars with high or low levels of allelopathy may respond differently to DIMBOA. RESULTS: In this study, we found that low concentrations of DIMBOA (≤ 0.06 mM) promoted seedling growth in allelopathic rice PI312777, while DIMBOA (≤ 0.08 mM) had no significant influence on the nonallelopathic rice Lemont. DIMBOA treatment caused changes in the expression of a large number of glutathione S-transferase (GST) proteins, which resulting in enrichment of the glutathione metabolic pathway. This pathway facilitates plant detoxification of heterologous substances. The basal levels of GST activity in Lemont were significantly higher than those in PI312777, while GST activity in PI312777 was slightly induced by increasing DIMBOA concentrations. Overexpression of GST genes (Os09g0367700 and Os01g0949800) in these two cultivars enhanced rice resistance to DIMBOA. CONCLUSIONS: Taken together, our results indicated that different rice accessions with different levels of allelopathy have variable tolerance to DIMBOA. Lemont had higher GST activity, which helped it tolerate DIMBOA, while PI312777 had lower GST activity that was more inducible. The enhancement of GST expression facilitates rice tolerance to DIMBOA toxins from barnyard grass root exudates.