MDA Accumulation Research Articles

Seed priming with cold plasma, iron, and manganese nanoparticles modulates salinity stress in hemp (Cannabis sativa L.) by improving germination, growth, and biochemical attributes.

Using cutting-edge technologies such as non-thermal plasma and metallic nanoparticles has shown promise in ameliorating salinity-induced stress in plants. However, there are still knowledge gaps concerning the most effective strategies for mitigating salinity stress in hemp (Cannabis sativa L.) plants. Consequently, this study was undertaken to investigate the impact of seed priming with cold plasma (CP), iron (Fe), and manganese (Mn) nanoparticles (NPs) on salinity modulation in hemp plants, aiming to improve seed germination, plant growth, and biochemical attributes. A pot experiment was conducted with salinity at three levels (0, 60, and 120 mM NaCl) and seed priming at five levels (control, 60 s CP, 90 s CP, 50 mg L-1 Fe NPs, and 50 mg L-1 Mn NPs). The results showed that salinity at 120 mM decreased germination percentage (GP, 34%), germination speed (GS, 61%), seedling vigor index (SVI, 47%), shoot weight (38%), root weight (15%), chlorophyll (Chl) a + b (31%), and relative water content (RWC, 24%) while increasing malondialdehyde (MDA, 48%) and proline (39%). Seed priming with CP, Fe NPs, and Mn NPs increased plant weight, GP, GS, SVI, RWC, and Chl but decreased MDA accumulation. Fe NPs and salinity at 60mM led to high levels of total phenolic content and total flavonoid content, which represent 29 and 44% increases, respectively, compared to the control. The heat map showed that among the treatments, GS and SVI had the highest degrees of variability. Fe NPs at 50mg L-1 and CP at 90s produced the best plant tolerance to salt stress.

25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens.

Broiler breeder hens allowed ad libitum (Ad) feed intake developed obesity and cardiac pathogenesis and thereby were susceptible to sudden death. A supplement of 69 µg 25-hydroxycholecalciferol (25-OH-D3)/kg feed rescued the livability of feed-restricted (R) and Ad-hens (mortality; 6.7% vs. 8.9% and 31.1% vs. 48.9%). Necropsy with the surviving counterparts along the time course confirmed alleviation of myocardial remodeling and functional failure by 25-OH-D3, as shown by BNP and MHC-β expressions, pathological hypertrophy, and cardiorespiratory responses (p < 0.05). 25-OH-D3 mitigated cardiac deficient bioenergetics in Ad-hens by rescuing PGC-1α activation, mitochondrial biogenesis, dynamics, and electron transport chain complex activities, and metabolic adaptions in glucose oxidation, pyruvate/lactate interconversion, TCA cycle, and β-oxidation, as well as in TG and ceramide accumulation to limit lipotoxic development (p < 0.05). Supplemental 25-OH-D3 also sustained Nrf2 activation and relieved MDA accumulation, protein carbonylation, and GSH depletion to potentiate cell survival in the failing heart (p < 0.05). Parts of the redox amendments were mediated via lessened blood hematocrit and heme metabolism, and improved iron status and related gene regulations (p < 0.05). In conclusion, 25-OH-D3 ameliorates cardiac pathological remodeling and functional compromise to rescue the livability of obese hens through metabolic flexibility and mitochondrial bioenergetics, and by operating at antioxidant defense, and heme and iron metabolism, to maintain redox homeostasis and sustain cell viability.

Delavinone elicits oxidative stress and triggers ferroptosis in colorectal cancer by inhibiting PKCδ-mediated phosphorylation of Nrf2

Ferroptosis is a potential therapeutic approach for colorectal cancer (CRC). Studies have shown that peimine and its analogs exhibit anti-cancer potential; however, the intricate relationship between ferroptosis and their efficacy in fighting CRC remains unclear. In this study, we attempted to assess the therapeutic impact of peimine and its analogs on CRC and unravel the underlying mechanisms. CRC cells and a DSS/AOM-induced CRC mouse model were employed for in vitro and in vivo experiments, molecular interactions and co-immunoprecipitation were used to identify target proteins. Among the compounds, delavinone significantly inhibited CRC cell proliferation and increased cellular lipid ROS levels, MDA accumulation, and GSH depletion; the ferroptosis inhibitors DFO and Fer-1 ameliorated delavinone-induced cell death. Mechanistically, delavinone impedes PKCδ-mediated Nrf2 phosphorylation by inhibiting the kinase activity of PKCδ, thereby decreasing Nrf2 nuclear translocation and downstream GSH synthesis-related gene expression. overexpression of GPX4 weakened the anticancer effect of delavinone, underscoring delavinone's inhibition of the PKCδ/Nrf2/GPX4 signaling axis and induction of ferroptosis in CRC cells. Consistent with in vitro findings, delavinone notably hindered AOM/DSS-induced colorectal carcinogenesis, exhibiting a pronounced pro-ferroptosis effect on CRC. This study delineates that delavinone exerts its anticancer activity by inducing ferroptosis through PKCδ inhibition, consequently reducing Nrf2 phosphorylation. These findings position delavinone as a promising candidate for CRC treatment.

A QTL on chromosome 17 identified by Genome-Wide Association Mapping controls postharvest cold tolerance of Cucurbita pepo L.

The worldwide cultivated Cucurbita pepo L. is one of the most diverse species in the plant kingdom. In this study, chilling tolerance over a wide range of cultivars was characterized to discover the allelic variants to improving the postharvest quality of the immature fruit during cold storage. For this purpose, fruits from 126 accessions of worldwide origin have been evaluated for weight loss and chilling injury after 3, 7 and 14 days of cold storage, classifying them into tolerant, partially tolerant, and sensitive accessions. To verify this classification, antioxidant capacity and lipid peroxidation (MDA) of contrasting accessions (tolerant vs. sensitive) were assessed. The antioxidant capacity significantly decreased during cold storage in the sensitive accessions, while it was maintained in tolerant accessions. Additionally, the sensitive accessions presented a higher accumulation of MDA during this period. Finally, a GWAS analysis using GBS data available in CuGenDBv2, combined with weight loss percentage data, led to the identification of a candidate QTL located on chromosome 17 that regulates postharvest cold tolerance in zucchini. The region contains four SNPs whose alternative alleles were significantly associated with lower weight loss percentage and chilling injury indices during cold storage. Two SNPs are located in the 3' UTR region of the gene CpERS1, a gene involved in ethylene perception. The other two SNPs generate missense mutations in the coding region of a Pectin methyl esterase inhibitor gene (CpPMI). The role of this QTL and these variants in chilling tolerance is discussed.

Genome-Wide Identification of Wheat USP Gene Family and Functional Dissection of TaUSP85 Involved in Heat Tolerance

A collection of conserved proteins known as universal stress protein (USP) is present in a wide range of species, including plants, fungi, bacteria, and animals. USPs are named for their ability to respond to a variety of stress conditions, such as heat stroke, osmotic stress, nutrient limitation, and exposure to toxins or antibiotics. While the USP response to different stress conditions in plants has been reported, little is known about the USP family in wheat (Triticum aestivum L.). In wheat, we identified 88 USP genes distributed across 21 chromosomes classified into four subfamilies. Phylogenetic tree and synteny analysis across multiple species revealed a highly conserved evolution of the USP family between monocots and dicots. Based on comparative analysis of protein domains, gene structure and conserved motifs, TaUSPs showed significant differences among the four subfamilies. Furthermore, expression pattern analysis of TaUSPs showed significant differences among various tissues and under different abiotic stress conditions. We further conducted transformation experiments with the TaUSP85 gene, which significantly enhanced yeast thermotolerance. Silencing of TaUSP85 through VIGS experiments in wheat resulted in significant wilting, decreased chlorophyll content, and increased MDA accumulation compared to control plants. The silenced plant lines had much more ROS accumulation than the control group, as determined by the findings of DAB and NBT staining. The interaction proteins TaUSP1 and TaUSP11 of TaUSP85 were screened by yeast two-hybrid and their interaction relationship was further verified by LCI. Overall, our findings enhance the comprehension of the USP gene family in wheat and provide a valuable resource for further investigation of these genes in wheat and related cereal crops.

Impact nano- and micro- form of CdO on barley growth and oxidative stress response

The objective was investigated the effects of CdO and nano-CdO as potential toxic pollutants on growth and redox response of barley. CdO and nano-CdO have been found to cause significant phytotoxicity in barley seedlings, with nano-CdO increasing plant tissue cadmium accumulation. This accumulation is linked to growth retardation and oxidative stress. Low molecular weight antioxidants like restored glutathione and ascorbate have been found to increase the activity of glutathione peroxidase (GPX), glutathione-S-transferase (GSTs), and ascorbate peroxidase (APX) in green tissues. Catalase (CAT) activity increased from 50 % with 100 mg/l CdO to 70 % with 1000 mg/l and nano-CdO. The observed disturbance in redox balance signals the upregulation of corresponding genes. Antioxidant enzyme isoform gene transcripts increased for SODB, CAT2, and APX. Cadmium buildup in root cells causes oxidative stress, leading to upregulation of SOD, CAT, GR, and GSTs isoform genes as well as protein carbonylation, sulfhydryl group degradation, and MDA accumulation. CdO and nano-CdO have similar phytotoxic effects, but bioavailability affects biochemical and molecular responses.

Arsenic induces ferroptosis in HTR-8/SVneo cells and placental damage

Placenta ferroptosis has been proven to be associated with a variety of adverse pregnancy outcomes. Arsenic, a conventional metal noxious substance, has garnered considerable attention due to traversing the placental barrier. How arsenic induces placental ferroptosis and reproductive developmental toxicities remains largely unknown. Herein, we investigated the impact of sodium arsenite (As (III)) on iron homeostasis in the placenta through both in vivo and in vitro experiments by using HTR-8/SVneo cells and ICR pregnant mice. As (III) up-regulated the expression of genes or proteins associated with iron uptake (TFRC, DMT1), iron storage (FTH, FTL), ferritin autophagy (NCOA4), and heme degradation (HO-1), and induced cell iron overload. Additionally, accumulation of the lipid hydroperoxide malondialdehyde within cells was triggered by As (III) through inhibition of the Nrf2/GPX4 signal pathway, which resulted in cellular ferroptosis. Fer-1 effectively alleviated the suppression of GPX4 induced by As (III), reduced the accumulation of intracellular lipid peroxidation product MDA, and mitigated cellular ferroptosis. As (III) affected the iron homeostasis, as evidenced by the abnormal iron accumulation in the placenta. Placental structural abnormalities and hemorrhage may be the reason for As (III) causing placental injury and subsequent poor pregnancy outcomes. This study provides new insights into understanding the mechanisms by which As (III) produces placental damage and possible fetal developmental toxicity.

Employing Titanium Dioxide Nanoparticles as Biostimulant against Salinity: Improving Antioxidative Defense and Reactive Oxygen Species Balancing in Eggplant Seedlings.

Salinity is a major abiotic stress that affects the agricultural sector and poses a significant threat to sustainable crop production. Nanoparticles (NPs) act as biostimulants and significantly mitigate abiotic stress. In this context, this experiment was designed to assess the effects of foliar application of titanium dioxide (TiO2) nanoparticles at 200 and 400 ppm on the growth of eggplant (Solanum melongena) seedlings under moderate (75 mM) and high (150 mM) salinity stress. The TiO2-NPs employed were characterized by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), thermal gravimetric analysis (TGA), and scanning electron microscopy (SEM) analysis. The seedlings were assessed physiologically, growth-wise, and biochemically. The seedlings were significantly affected by their physiological attributes (Fv'/Fm', Fv/Fm, NPQ), growth (root length, shoot length, number of leaves, fresh biomass, dry biomass, leaf greenness), antioxidative enzymes (SOD, POD, CAT, APx, GR), stress indicators (H2O2, MDA), and toxic ion (Na+) concentrations. The maximum decrease in physiological and growth attributes in eggplant seedling leaves was observed with no TiO2-NP application at 150 mM NaCl. Applying TiO2-NPs at 200 ppm showed significantly less decrease in Fv'/Fm', root length, shoot length, number of leaves, fresh biomass, dry biomass, and leaf greenness. In contrast, there were larger increases in SOD, POD, CAT, APx, GR, and TSP. This led to less accumulation of H2O2, MDA, and Na+. No significant difference was observed in higher concentrations of TiO2-NPs compared to the control. Therefore, TiO2-NPs at 200 ppm might be used to grow eggplant seedlings at moderate and high salinity.

Se-Methylselenocysteine Ameliorates DEHP-Induced Ferroptosis in Testicular Sertoli Cells via the Nrf2/GPX4 Axis.

Di (2-ethylhexyl) phthalate (DEHP) is an important plasticizer in industrial production, and its toxic effects on testes are widely recognized. Se-methylselenocysteine (SMC) is a major selenium compound found in selenium-rich plants, which possesses unique biological properties such as antioxidants. However, the effect of SMC on DEHP-induced testicular injury and the specific mechanism remains unknown. In this study, 50 mice were randomly divided into 5 groups and were given corn oil (Control), DEHP, low-dose SMC (L-SMC), moderate-dose SMC (M-SMC), or high-dose SMC (H-SMC). The sperm quality of the mice in each group was determined, and HE staining and transmission electron microscopy (TEM) were applied to observe testicular morphology, and testicular tissues were collected for the subsequent molecular biological analyses. The TM4 cell line was applied in vitro for mechanism validation. Our results showed that DEHP could lead to decreased sperm quality and blood-testis barrier damage in mice, which could be alleviated by SMC. Mitochondrial damage accompanied by accumulation of total iron content, MDA, and 4-HNE, as well as downregulation of antioxidants SOD, GSH, and GSH-Px were observed after DEHP treatment, which exhibited a typical ferroptosis feature. In vitro experiments confirmed that SMC promoted upregulation of GPX4 in TM4 cells and was able to alleviate DEHP metabolite MEHP-induced ferroptosis and promote the expression of cell junction key proteins ZO-1, Occludin, and Connexin 43, which could be inhibited by the GPX4 inhibitor RSL3 or the Nrf2 inhibitor ML385. Overall, the above results suggest that SMC ameliorates the DEHP-induced ferroptosis in testicular Sertoli cells, protects the blood-testis barrier, and prevents sperm aberrations via the Nrf2/GPX4 axis.

New insights into evodiamine attenuates IPEC-J2 cells pyroptosis induced by T-2 toxin - Activating Keap1-Nrf2/NF-κB signaling pathway through binding with Keap1

T-2 toxin (T-2) is a highly toxic mycotoxin with a molecular weight of 466.52 g/mol. Evodiamine (EV), an alkaloid component of Evodia, has anti-inflammation and antioxidant properties. As a receptor of oxidative stress, Keap1 with a molecular weight of 70 kDa, is a molecular switch that controls the Nrf2 signaling pathway. In this paper, the effect of EV on Keap1-Nrf2/NF-κB pathway was investigated. Based on our research outcomes, it was observed that T-2 exposure substantially increased IPEC-J2 cells intracellular ROS levels and MDA accumulation, decreased SOD and CAT activities, disrupted intestinal tight junction (ZO-1, occludin, and claudin-1), and up-regulated pyroptosis-related protein (ASC, NLRP3, caspase-1, GSDMD, IL-1β, and IL-18). Additionally, EV could bind well with Keap1, the separating it from Nrf2, promoting Nrf2 into the nucleus, enhanced antioxidant enzyme activities, reduced the production of ROS, down-regulated NF-κB expression, alleviated T-2-induced pyroptosis, and restored tight junction protein expression. However, after treatment with the Nrf2 inhibitor ML385, ML385 reversed the protective effect of EV on IPEC-J2 cells. Collectively, EV can activate the Keap1-Nrf2/NF-κB signaling pathway via binding to Keap1, exert anti-inflammatory and antioxidant effects, inhibit the pyroptosis of IPEC-J2 cells triggered by T-2, and retore intestinal barrier function.

Baicalin enhances antioxidant, inflammatory defense, and microbial diversity of yellow catfish (Pelteobagrus fulvidraco) infected with Aeromonas hydrophila.

The aim of this research was to clarify the mechanism through which baicalin exerts its inhibitory effects on Aeromonas hydrophila infection. The antibacterial efficacy of baicalin was assessed by determining its minimum inhibitory concentration (MIC) against A. hydrophila. Various parameters, including the growth curve, cell wall integrity, biofilm formation, AKP content, and morphological alterations of A. hydrophila, were analyzed. In vivo experiments involved the administration of A. hydrophila 4 h postintraperitoneal injection of varying doses of baicalin to induce infection, with subsequent monitoring of mortality rates. After a 3 d period, liver, spleen, and intestinal tissues were harvested to evaluate organ indices, antioxidant and immune parameters, as well as intestinal microbial composition. The findings indicated that baicalin treatment resulted in the disruption of the cell wall of A. hydrophila, leading to the loss of its normal structural integrity. Furthermore, baicalin significantly inhibited biofilm formation and facilitated the release of intracellular proteins (P < 0.05). In vivo, baicalin enhanced the survival rates of yellow catfish infected with A. hydrophila. Compared to the control group, the liver index of yellow catfish was elevated, while the spleen and intestinal indices were reduced in the baicalin-treated group (P < 0.05). Additionally, baicalin at an appropriate dosage was found to increase levels of SOD, GSH, CAT, ACP, and AKP in yellow catfish (P < 0.05), while simultaneously decreasing MDA accumulation and the mRNA expression of inflammatory markers such as Keap1, IL1, IFN-γ, and TNF-α, (P < 0.05). Moreover, baicalin significantly enhanced the operational taxonomic unit (OTU) count in A. hydrophila-infected yellow catfish (P < 0.05), restoring the abundance of Barnesiellaceae, Enterobacteriaceae, Plesiomonas, and UBA1819 (P < 0.05). In summary, baicalin demonstrates the potential to improve the survival rate of yellow catfish subjected to A. hydrophila infection, augment antioxidant and immune responses, mitigate inflammation, and enhance intestinal microbial diversity.

Chronic UVB exposure induces hepatic injury in mice: Mechanistic insights from integrated multi-omics

Chronic UVB exposure poses a significant threat to both skin and visceral health. In recent years, the adverse role of chronic UVB exposure in liver health has been suggested but not fully elucidated. This study aims to comprehensively investigate the effects of chronic UVB exposure on liver health in male SKH-1 hairless mice and clarify potential mechanisms through multi-omics approaches. The findings suggested that 10-week chronic skin exposure to UVB not only triggers hepatic inflammation and oxidative stress but also, more importantly, results in lipid metabolism abnormalities in the liver. Hepatic transcriptomic analysis revealed significant alterations in various signaling pathways and physiological processes associated with inflammation, oxidative stress, and lipid metabolism. Further lipidomic analysis illustrated significant changes in the metabolism of glycerolipids, sphingolipids, and glycerophospholipids in the liver following chronic UVB exposure. The 16S rRNA sequencing analysis indicated that chronic UVB exposure disrupts the structure and function of the microbiota. In search of potential mechanisms used by the microbiome to regulate the hepatic disease morphology, we filtered mouse fecal supernatants and cultured the supernatants with HepG2 cells. Fecal supernatant from UVB-exposed mice induced increased secretion of the inflammatory cytokine IL-8, accumulation of MDA, reduced SOD activity, and decreased lipid content in normal hepatic cells. In summary, skin chronic exposure to UVB induces multiple liver injuries and gut microbiota dysbiosis in mice and gut microbiota metabolites may be one of the contributing factors to hepatic injury caused by chronic UVB exposure. These discoveries deepen the comprehension of the health risks associated with chronic UVB exposure.

Assessment of the Modifying Effect of Zinc and Copper on Toxic Stress of Barley Plants Caused by Cadmium

In a vegetation experiment on sod-podzolic sandy loam soil with Cd2+ addition at doses of 25 and 45 mg/kg, we studied how the response of barley plants to the toxic effects of cadmium changes if various amounts of heavy metals (HM) with the functions of trace elements were introduced together with it, using the example of zinc and copper. In addition, several variants were laid, in which copper and zinc were also introduced along with cadmium. Thus, doses and combinations of metals were used in the experiment: Cd45, Cd25Cu50, Cd25Cu100, Cd25Cu100, Cd25Cu200, Cd45Cu50, Cd45Cu100, Cd45Cu200, Cd45Zn50, Cd45Zn100, Cd45Zn150. Morphometric parameters (appearance, height of plants, their biomass and leaf area), biochemical parameters (accumulation of MDA, total antioxidants and crude protein), crop structure (straw weight, grain weight, 1000 grain weight) were evaluated in experimental plants. In addition, the gross content of HM and other elements in the soil and their transition to the soil solution were analyzed. It is shown that the introduction of cadmium alone led to a significant inhibition of the growth and development of barley plants. At the same time, the combined addition of HM trace elements with cadmium significantly modified the effect of cadmium. Zinc contributed to a decrease in the toxic effects of cadmium, and the intensity of this effect increased as the concentration of zinc increased, and the toxic effects of this HM at the doses considered had not yet manifested themselves. Copper, as a more toxic element, showed its stimulating effect at lower doses than zinc, and at higher doses, the development of acute stress caused by the combined toxic effects of 2 HM was observed. This is true for a dose of cadmium of 45 mg/kg, with a lower dose of cadmium (25 mg/kg), copper had a greater stimulating effect. The considered effects were primarily noted when evaluating morphometric indicators and productivity. Based on the biochemical parameters, it was not possible to draw clear conclusions about how the addition of zinc and copper changed the effects of cadmium. Apparently, it was more appropriate to use other biochemical parameters to assess stress effects. It was noted that the introduction of trace elements generally contributed to a reduction in the accumulation of cadmium in the aboveground biomass of barley plants, however, the addition of zinc led to an increased transition of cadmium into straw, but not into grain.

The transcription factor TabZIP156 acts as a positive regulator in response to drought tolerance in Arabidopsis and wheat (Triticum aestivum L.)

Drought stress strongly restricts the growth, development, and yield of wheat worldwide. Among the various transcription factors (TFs) involved in the wheat drought response, the specific functions of many basic leucine zipper (bZIP) TFs related to drought tolerance are still not well understood. In this study, we focused on the bZIP TF TabZIP156 in wheat. Our analysis showed that TabZIP156 was highly expressed in both roots and leaves, and it responded to drought and abscisic acid (ABA) stress. Through subcellular localization and transactivation assays, we confirmed that TabZIP156 was located to the nucleus and functioned as a transcriptional activator. Overexpression of TabZIP156 in Arabidopsis enhanced drought tolerance, as evidenced by higher germination rate, longer root length, lower water loss rate, reduced ion leakage, increased proline accumulation, decreased levels of H2O2, O2− and MDA, and improved activities of POD, SOD, and CAT enzymes. Additionally, the expression of drought- and antioxidant-related genes were significantly upregulated in TabZIP156 transgenic Arabidopsis under drought stress. However, silencing TabZIP156 in wheat led to decreased proline content, increased accumulation of H2O2, O2− and MDA, reduced activities of antioxidant enzymes, and downregulation of many drought- and antioxidant-related genes under drought stress. Furthermore, the dual-luciferase assay demonstrated that TabZIP156 could activate the expression of TaP5CS, TaDREB1A, and TaPOD by binding to their promoters. Taken together, this study highlights the significant role of TabZIP156 in drought stress and provides valuable insights for its potential application in breeding drought-resistant wheat.

First Peek into the Transcriptomic Response in Heat-Stressed Tomato Inoculated with Septoglomus constrictum.

In this study, we report the interaction between an arbuscular mycorrhizal fungus, Septoglomus constrictum, and tomato plants under heat stress. For the first time, this interaction was studied by Illumina RNA-seq, followed by a comprehensive bioinformatic analysis that investigated root and leaf tissue samples. The genome-wide transcriptional profiling displayed fewer transcriptomic changes in the root under heat-stress conditions caused by S. constrictum. The top 50 DEGs suggested significant changes in the expression of genes encoding heat-shock proteins, transporter proteins, and genes of phytohormone metabolism involving jasmonic acid signalling. S. constrictum induced the upregulation of genes associated with pathways such as 'drought-responsive' and the 'development of root hair' in the root, as well as 'glycolipid desaturation', 'intracellular auxin transport', and 'ethylene biosynthesis' in the leaf. The pathways 'biotin biosynthesis' and 'threonine degradation' were found in both investigated tissue types. Expression analysis of transcription factors showed 2 and 11 upregulated transcription factors in heat-stressed root and leaf tissues, respectively. However, we did not find shared transcription factors. Heat-stressed arbuscular mycorrhizal plants suffered less oxidative stress when exposed to high temperatures. Colorimetric tests demonstrated less accumulation of H2O2 and MDA in heat-stressed mycorrhizal plants. This phenomenon was accompanied by the higher expression of six stress genes that encode peroxidases, glutathione S-transferase and ubiquitin carboxyl-terminal hydrolase in roots and leaves. Our findings provide a new perspective on elucidating the functional metabolic processes of tomato plants under mycorrhizal-heat stressed conditions.

High-fat intake induces gut microbiota disorders, inflammatory responses and oxidative stress in Nyctereutes procyonoides

The Nyctereutes procyonoides is highly regarded in the farming and leather industries because of the high value of its fur, which renders artificial feeding a crucial aspect. However, high-fat diets have always been associated with a variety of digestive disorders. This study aimed to investigate the impact of high-fat diets on the gut microbiota and the mechanisms of gut damage in Nyctereutes procyonoides. 16S rRNA sequencing demonstrated that high-fat diets caused diarrhea and intestinal damage through alterations in the gut microbiota: a decrease in the abundance of Firmicutes, an increase in the abundance of Proteobacteria and Actinobacteria, and an increase in the abundance of Enterococcaceae, Escherichia coli-Shigella, Clostridium and Lactobacillus. Subsequently, changes in metabolic pathways, such as amino and fatty acid pathways, were identified by KEGG and COG enrichment analysis, and the TLR4/NF-κB/NLRP3 inflammatory signaling pathway was shown to be activated by high-fat diets. In addition, high-fat diets lead to the accumulation of ROS and MDA and reduce the activity of the antioxidant enzymes GSH-PX and SOD. Correspondingly, the levels of proinflammatory cytokines (IL-6, IL-1β and TNF-α) were significantly increased, and the apoptosis and necrosis signaling pathways of colonic cells were detected, causing a dramatic decrease in the expression of intestinal tight junction proteins (Occludin, E-cadherin, ZO-1 and ZO-2). In conclusion, high-fat diets altered the structure of the Nyctereutes procyonoides gut microbiota community and led to colon damage. This study provides new insights into the intestinal health of Nyctereutes procyonoides.Graphical

Research on the Isolation of Endophytic Fungi from Papaya and the Prevention of Colletotrichum gloeosporioides.

Endophytic fungi can be used as a source of herbal antioxidants to overcome the limitations of low yield and lengthy growth cycles associated with using plants as raw materials for antioxidant production. Papaya fruit is often susceptible to infection by Colletotrichum gloeosporioides after harvest, leading to postharvest rot. Endophytic fungi were extracted with ethyl acetate, and the initial screening concentration was 100 mg/L. Seven strains were identified, with scavenging rates exceeding 50% and strong antioxidant activity. The IC50 values in DPPH and ABTS free radical scavenging assays ranged from 19.72 to 84.06 mg/L and from 14.34 to 64.63 mg/L, respectively. Strain Y17 exhibited robust antioxidant activity (IC50 < 20 mg/L) and was identified as Penicillium rolfsii (MT729953) through ITS sequencing. Treatment of papaya fruit wounds with a fermentation broth of strain Y17 significantly inhibited the infection and colonization of anthracnose pathogens, resulting in a slowed disease incidence rate. This promoted the activity of protective enzymes, such as CAT, POD, and SOD, in the papaya fruit and slowed down the rate of MDA accumulation. This strain, which was found to have antioxidant activity in this study, has the potential to control anthracnose in papaya and has value in terms of further development and utilization.

Quercetin antagonizes apoptosis, autophagy and immune dysfunction induced by di(2-ethylhexyl) phthalate via ROS/ASK1/JNK pathway

Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer that can damage various organizations and physiques through oxidative stress. Quercetin (Que) is a rich polyphenol flavonoid with good anti-inflammatory and antioxidant effects. However, the protection mechanism of Que against DEHP exposure-induced IPEC-J2 cell injury and the implication of autophagy, apoptosis and immunity are still unclear. In this experiment, we looked into the toxicity regime of DEHP exposure on IPEC-J2 cells and the antagonistic function of Que on DEHP. In the experiment, 135 μM DEHP and/or 80 μM Que were used to treat the IPEC-J2 cells for 24h. Experiments indicated that DEHP exposure can cause increased reactive oxygen species (ROS) levels leading to oxidative stress, decreased CAT, T-AOC and GSH-Px activities, increased MDA and H2O2 accumulation, activated the ASK1/JNK signalling pathway, and further increases in the levels of apoptosis markers Bax, Caspase3, Caspase9, and Cyt-c, while reduced the Bcl-2 expression. DEHP also increased the expression of genes linked to autophagy (ATG5, Beclin1, LC3), while decreasing the expression of P62. Additionally, DEHP exposure led to elevated levels of IL1-β, IL-6, MCP-1, and TNF expression. When exposed to Que alone, there were no significant changes in cellular oxidative stress level, ASK1/JNK signalling pathway expression level, apoptosis, autophagy and cellular immune function. The combination of DEHP and Que treatment remarkably decreased the proportion of autophagy and apoptosis, and recovered cellular immunity. In summary, Que can attenuate DEHP-induced apoptosis and autophagy in IPEC-J2 cells by regulating the ROS/ASK1/JNK signalling pathway and improving the immune dysfunction of IPEC-J2 cells.

6-BA Reduced Yield Loss under Waterlogging Stress by Regulating the Phenylpropanoid Pathway in Wheat.

Waterlogging stress causes substantial destruction to plant growth and production under climatic fluctuations globally. Plants hormones have been widely explored in numerous crops, displaying an imperative role in crop defense and growth mechanism. However, there is a paucity of research on the subject of plant hormones regulating waterlogging stress responses in wheat crop. In this study, we clarified the role of 6-BA in waterlogging stress through inducing phenylpropanoid biosynthesis in wheat. The application of 6-BA (6-benzyladenine) enhanced the growth and development of wheat plants under waterlogging stress, which was accompanied by reduced electrolyte leakage, high chlorophyll, and soluble sugar content. ROS scavenging was also enhanced by 6-BA, resulting in reduced MDA and H2O2 accumulation and amplified antioxidant enzyme activities. Additionally, under the effect of 6-BA, the acceleration of lignin content and accumulation in the cell walls of wheat tissues, along with the activation of PAL (phenylalanine ammonia lyase), TAL (tyrosine ammonia lyase), and 4CL (4-hydroxycinnamate CoA ligase) activities and the increase in the level of transcription of the TaPAL and Ta4CL genes, were observed under waterlogging stress. Also, 6-BA improved the root growth system under waterlogging stress conditions. Further qPCR analysis revealed increased auxin signaling (TaPR1) in 6-BA-treated plants under waterlogging stress that was consistent with the induction of endogenous IAA hormone content under waterlogging stress conditions. Here, 6-BA also reduced yield loss, as compared to control plants. Thus, the obtained data suggested that, under the application of 6-BA, phenylpropanoid metabolism (i.e., lignin) was stimulated, playing a significant role in reducing the negative effects of waterlogging stress on yield, as evinced by the improved plant growth parameters.

New insights into azelaic acid-induced resistance against Alternaria Solani in tomato plants

BackgroundThe effect of azelaic acid (Aza) on the response of tomato plants to Alternaria solani was investigated in this study. After being treated with Aza, tomato plants were infected with A. solani, and their antioxidant, biochemical, and molecular responses were analyzed.ResultsThe results demonstrated that H2O2 and MDA accumulation increased in control plants after pathogen infection. Aza-treated plants exhibited a remarkable rise in peroxidase (POD) and catalase (CAT) activities during the initial stages of A. solani infection. Gene expression analysis revealed that both Aza treatment and pathogen infection altered the expression patterns of the SlNPR1, SlERF2, SlPR1, and SlPDF1.2 genes. The expression of SlPDF1.2, a marker gene for the jasmonic acid/ethylene (JA/ET) signaling pathway, showed a remarkable increase of 4.2-fold upon pathogen infection. In contrast, for the SlNPR1, a key gene in salicylic acid (SA) pathway, this increased expression was recorded with a delay at 96 hpi. Also, the phytohormone analysis showed significantly increased SA accumulation in plant tissues with disease development. It was also revealed that tissue accumulation of JA in Aza-treated plants was increased following pathogen infection, while it was not increased in plants without pathogen inoculation.ConclusionThe results suggest that the resistance induced by Aza is mainly a result of modulations in both SA and JA pathways following complex antioxidant and molecular defense responses in tomato plants during A. solani infection. These findings provide novel information regarding inducing mechanisms of azelaic acid which would add to the current body of knowledge of SAR induction in plants as result of Aza application.