Enzyme Activity Research Articles

Determinants of rhizospheric organic carbon fractions and accumulation in four different vegetations of coastal saline-alkali soils

Rhizosphere processes are key pathways through which plants influence the carbon cycling of diverse ecosystems and are closely associated with vegetation types. However, the environmental responses of rhizospheric soil organic carbon (SOC) mediated by the interaction between rhizospheric effect and vegetation type remain uncertain, severely limiting our assessment of the carbon sequestration potential of different coastal vegetation. Here, we identified the core factors driving changes in various soil carbon fractions in the rhizosphere of four coastal vegetation types by testing the contents of the reactive, dissolved, particulate, mineral-associated, heavy and light fractions of SOC and their relationships with physicochemical properties and enzyme activities. It was found that the rhizosphere effect significantly influenced SOC, with rhizospheric SOC contents varying significantly among vegetation types, ranging from 2.12 to 9.04 g/kg. Besides, rhizospheric soil pH was found to contribute significantly to SOC fractions (except for light organic carbon) and exert significant inhibitory effects on SOC, reactive organic carbon, mineral-associated organic carbon and heavy organic carbon. Despite the different responses of various SOC fractions to physicochemical properties and enzyme activities, soil available phosphorus and alkaline phosphatase activity emerged as core environmental factors influencing rhizospheric SOC accumulation across different coastal vegetation types. This study presents a promising framework for understanding the determinants of SOC fractions in rhizospheric soil, and their accumulation in the vegetation of coastal saline-alkali soils. In addition to alkalinity, phosphorus acquisition capacity can be a key predictor of coastal SOC fractions and their accumulation.

Functional significance of CYP2B6 gene rare allelic variants identified in Japanese individuals

Cytochrome P450 2B6 (CYP2B6) catalyzes the metabolism of many drugs, including efavirenz and propofol. Genetic polymorphisms in CYP2B6 alter its enzymatic activity and substantially affect its pharmacokinetics. High-frequency variants, such as CYP2B6*6, are associated with the risk of developing side effects due to reduced CYP2B6 activity. However, the impact of rare alterations on enzyme function remains unknown, and some of these variants may significantly decrease the CYP2B6 activity. Therefore, in this study, we evaluated in vitro the functional alterations in 29 missense variants of the CYP2B6 gene identified in 8,380 Japanese individuals. Wild-type CYP2B6 and 29 rare CYP2B6 variants were transiently expressed in mammalian cells. The expression levels of variant CYP2B6 proteins in the microsomal fractions extracted from 293FT cells were assessed using western blotting and reduced-carbon monoxide difference spectroscopy, and a specific peak at 450 nm was detected in the wild-type and 19 variants. Furthermore, kinetic parameters were determined by assaying the reactions with efavirenz and propofol and quantifying the metabolite concentrations. We found that 12 variants had significantly lower or abolished enzymatic activity with both the substrates. In silico three-dimensional docking and molecular-dynamics simulations suggested that these functional changes were due to conformational changes in essential regions, such as the heme-binding site and ligand channels involved in transporting substrates to the active site. These findings have implications for predicting the plasma concentrations of CYP2B6 substrates and controlling their side effects.

Perturbation of Enzyme Structure by nano-Metal Organic Frameworks: A Question Mark on their Safety-by-Design?

Our study investigates the interactions between nanoscale Metal-Organic Frameworks (nMOFs), specifically ZIF-8 and CuIm, and key enzymes: Acetylcholine Esterase (AChE), α-amylase. Using circular dichroism (CD) spectroscopy, we observed significant alterations in the secondary structures of these enzymes upon interaction with nMOFs. AChE showed a reduction in α-helix content from 20.1% to a significantly lower value when exposed to 160µg/mL of nMOFs, with a corresponding increase in β-sheet and other structural components. Enzymatic activity assays revealed that CuIm nMOFs decreased AChE activity by 67.08% at the highest concentration tested (160µg/mL). ZIF-8 also affected AChE activity significantly at this concentration. Similarly, α-amylase exhibited structural changes, with increasing concentrations of nMOFs leading to a near-total loss of secondary structure at 80 and 160µg/mL. These structural changes were accompanied by a marked decrease in enzymatic activity, particularly with CuIm nMOFs showing the most substantial inhibitory effects. Our findings highlight the profound impact of nMOFs on enzyme structure and function, emphasising the need for comprehensive assessments of nMOFs' potential toxicity and understanding the aspects of their safety-by-design.

Impacts of prescribed fire and mechanical shredding of aboveground vegetation for fire prevention on ecosystem properties, structure, functions and overall multi-functionality of a semi-arid pine forest

Ecosystem multi-functionality is a key concept when measured to protect forests from natural and anthropogenic disturbances, such as fire prevention techniques, must be adopted. Despite this importance, scarce studies have analysed the impacts of prescribed burning and aboveground vegetation management on ecosystem functions and overall multi-functionality. To fill this gap, this study has evaluated the changes in some ecosystem properties and structure (associated with soil characteristics and plant diversity, respectively), in important forest functions, and the overall ecosystem multi-functionality in a Mediterranean pine forest of Castilla La Mancha (Central Eastern Spain) under three site conditions: (i) undisturbed ecosystem; (ii) forest subjected to mechanical shredding of aboveground vegetation (hereafter “AVMS”); and (iii) forest treated as above and then with prescribed fire (“AVMS + PF”). The results of the study have shown that neither the PF nor AVMS have significantly modified the structure, properties and functions as well as the overall multi-functionality of the forest ecosystem. These slight impacts of the treatments are due to the low fire severity of the prescribed burning and the long time elapsed from the vegetation management. Among the studied ecosystem functions, organic matter decomposition (driven by the enzymatic activities and soil basal respiration), water cycle (influenced by soil water content and water infiltration), carbon stock (linked to soil organic matter) and biomass production decreased, when species richness and plant diversity increased. The study is useful to indicate the feasibility of forest management actions for fire prevention in delicate forest ecosystems of the Mediterranean environments.

HDAC1 promotes basal autophagy and proliferation of colorectal cancer cells by mediating ATG16L1 deacetylation

Autophagy is an evolutionarily conserved degradation pathway for maintaining cellular homeostasis and its dysregulation leads to numerous human diseases such as cancer. As a core protein for autophagy, ATG16L1 (autophagy related 16 like 1 ) is heavily regulated by post-translational modifications, including phosphorylation, ubiquitination, and methylation, which is critical for autophagy regulation. In this study, we identify HDAC1 (histone deacetylase 1) as a regulator of ATG16L1 acetylation and hence autophagy. Specifically, HDAC1 colocalizes and interacts with ATG16L1, and reduces its acetylation, which is highly dependent on its enzymatic activity. By promoting ATG16L1 deacetylation, HDAC1 enhances ATG16L1 interaction with the ATG12-ATG5 conjugate, resulting in the activation of autophagic pathway. Consistently, the induction of basal autophagy by HDAC1 in colorectal cancer cells largely relies on its deacetylase activity as well as ATG16L1. Moreover, HDAC1 enhances the survival, proliferation, and transformation of colorectal cancer cells in an ATG16L-dependent manner, indicating the fundamental roles of autophagy in colorectal cancer. Together, our findings uncover a novel regulatory mechanism of autophagy and suggest both HDAC1 and ATG16L1 as therapeutic targets for colorectal cancer.

Age-dependent haemogram and sex-dependent serum biochemistry values in semi-feral Konik horses.

Semi-feral, free-roaming Konik polski horses are used in some European countries for preserving semi-open pasture landscapes. The estimation of their health status is still limited by insufficient data on various blood parameters. Therefore, our study aimed at the sex- and age-dependent analysis of haemogram and selected biochemistry parameters in healthy, semi-feral Koniks. In order to reach this aim, we took blood samples from 53 female and 18 male (8 uncastrated, 10 castrated) Koniks living in two Middle German nature reserves. They were of different age (9-266 months) and without signs of illness. Blood samples were analysed by an accredited laboratory. We identified age- but not sex-dependent changes in the white blood cell count (WBC). Higher age mainly caused a decrease in lymphocytes. Therefore, WBC correlated negatively and granulocyte-to-lymphocyte ratio positively with increasing age. Serum values of selected biochemical parameters did not depend on age but showed some sex-related differences. In this regard, serum total protein, triglyceride and the enzymatic activities of alkaline phosphatase, aspartate transaminase and g-glutamyltransferase were higher in males than females. However, the sex dependency of these enzymatic activities was restricted to uncastrated males. They also showed higher serum values for calcium and selenium than castrated males or all females. As far as the respective group sizes permitted, we then calculated age- or sex-dependent reference interval values for all parameters analysed. These values improve now the estimation of the health status of semi-feral, free-roaming Konik horses and provide a stable basis for future studies.

Metabolic activation of WHO-congeners PCB28, 52, and 101 by human CYP2A6: evidence from in vitro and in vivo experiments.

Despite extensive research on the metabolism of polychlorinated biphenyls (PCBs), knowledge gaps persist regarding their isoform-specific biotransformation pathways. This study aimed to elucidate the role of different cytochrome P450 enzymes in PCB metabolism, focusing on WHO-congeners 2,4,4'-trichlorobiphenyl (PCB28), 2,2',5,5'-tetrachlorobiphenyl (PCB52), and 2,2',4,5,5'-pentachlorobiphenyl (PCB101). Utilizing engineered HEK293 cell lines, we investigated the in vitro metabolism of these PCBs by CYP1A2, CYP2C8, CYP2C9, CYP3A4, CYP2A6, and CYP2E1, revealing robust production of hydroxylated metabolites. Our results show that CYP2A6 plays a major role in the metabolism of these congeners responsible for predominant formation of para-position hydroxylated metabolites, with concentrations reaching up to 1.61µg/L (5,89nM) for PCB28, 316.98µg/L (1,03µM) for PCB52, and 151.1µg/L (441nM) for PCB101 from a 20µM parent PCB concentration. Moreover, concentration-dependent cytotoxic and cytostatic effects induced by reactive intermediates of the PCB hydroxylation pathway were observed in HEK293CYP2A6 cells, for all three congeners tested. CYP2A6 was specifically capable of activating PCBs 28 and 101 to genotoxic metabolites which produced genetic defects which were propagated to subsequent generations, potentially contributing to carcinogenesis. In a clinical study examining CYP2A6 enzyme activity in formerly exposed individuals with elevated internal PCB levels, a participant with increased enzyme activity showed a direct association between the phenotypic activity of CYP2A6 and the metabolism of PCB28, confirming the role of CYP2A6 in the in vivo metabolism of PCB28 also in humans. These results altogether reinforce the concept that CYP2A6 plays a pivotal role in PCB congener metabolism and suggest its significance in human health, particularly in the metabolism of lower chlorinated, volatile PCB congeners.

Reseeding increased plant biomass production and soil fertility, but not plant species diversity in degraded grasslands in China

Reseeding is a primary measure to restore degraded grasslands. Numerous studies have conducted experiments to investigate how the properties of grassland ecosystems respond to reseeding in China. However, there is a lack of summary of the results of these studies. Here, we conducted a hierarchical random-effects meta-analysis on the effects of reseeding on plant, soil, and microbial properties. We collected 19 variables, including plant biomass, species diversity and richness, soil organic carbon content, soil total and available nutrients, soil water content, soil microbial biomass and diversity, and enzyme activity, from a dataset of 1363 paired observations (degraded vs. reseeded) from 75 publications. The results showed that reseeding increased aboveground and belowground plant biomass by 70.2% and 68.0% on average, respectively. Reseeding increased soil organic carbon, phosphorus, and potassium contents, but did not affect soil nitrogen levels. Reseeding increased soil microbial nitrogen under conditions of tillage and fertilization. Reseeding age was found to have a positive correlation with species richness, while planting type, fertilization, and tillage did not have a significant impact on the species richness and diversity. Under the treatments of fertilization, non-tillage, and mix-planting, the response ratio of aboveground biomass to reseeding was positively correlated with the response ratio of species diversity to reseeding. Our results concluded that current reseeding practices can significantly improve plant biomass production and soil fertility but have minor effects on plant species diversity. These findings indicate that the preservation of biodiversity should receive greater attention from both researchers and practitioners in grassland remediation in China.

Effects of different microplastic types on soil physicochemical properties, enzyme activities, and bacterial communities

Global concern continues to mount regarding the accumulation of microplastics (MPs) in soil. However, little is known about how various types of MPs influence the properties of soil ecosystems. Here, we evaluated the effects of six different types of MPs, including low-density polyethylene (LDPE), polyamide (PA), polystyrene (PS), polyhydroxy-alkanoates (PHA), polybutadiene styrene (PBS), and polylactide (PLA), on soil physicochemical properties, enzyme activities, and microbial communities. At the end of a 230-day soil incubation, we observed significant changes in soil moisture content, soil organic carbon, pH, NH4+-N, NO3--N, and available phosphorus. The addition of MPs had a significant influence on the activities of soil β-glucosidase, acid phosphatase, urease, and fluorescein diacetate hydrolase, with effects varying with MP type. Results of 16S rRNA gene high throughput sequencing showed that MP exposure had little effect on soil microbial alpha diversity, but that PHA contamination significantly reduced ACE, Chao1, and Shannon index values. MP contamination also altered soil microbial community composition. In particular, the relative abundance of Firmicutes increased significantly while the relative abundance of Actinobacteriota, Proteobacteria (especially the nitrogen-fixing rhizobia), and Acidobacteriota decreased following exposure to PHA. Redundancy analysis showed that acid phosphatase and pH were the two main environmental factors affecting bacterial community structure at the phylum and order levels. Furthermore, Tax4Fun2 analysis found that MP treatment disrupted fundamental bacterial metabolic pathways. Our findings indicate that different types of MPs can affect soil fertility, bacterial community structure, and function in various ways, and highlight that biodegradable MPs may alter soil bacterial communities more than conventional MPs.

Taurocholic acid represents an earlier and more sensitive biomarker and promotes cholestatic hepatotoxicity in ANIT-treated rats.

Bile acid homeostasis is crucial for the normal physiological functioning of the liver. Disruptions in bile acid profiles are closely linked to the occurrence of cholestatic liver injury. As part of our diagnostic and therapeutic approach, we aimed to investigate the disturbance in bile acid profiles during cholestasis and its correlation with cholestatic liver injury. Before the occurrence of liver injury, alterations in bile acid profiles were detected in both plasma and liver between 8 and 16 h, persisting up to 96 h. TCA, TCDCA, and TUDCA in the plasma, as well as TCA, TUDCA, TCDCA, TDCA, TLCA, and THDCA in the liver, emerged as early sensitive and potential markers for diagnosing ANIT-induced cholestasis at 8-16 h. The distinguishing features of ANIT-induced liver injury were as follows: T-BAs exceeding G-BAs and serum biochemical indicators surpassing free bile acids. Notably, plasma T-BAs, particularly TCA, exhibited higher sensitivity to cholestatic hepatotoxicity compared with serum enzyme activity and liver histopathology. Further investigation revealed that TCA exacerbated ANIT-induced liver injury by elevating liver function enzyme activity, inflammation, and bile duct proliferation and promoting the migration of bile duct epithelial cell. Nevertheless, no morphological changes or alterations in transaminase activity indicative of liver damage were observed in the rats treated with TCA alone. Additionally, there were no changes in bile acid profiles or inflammatory responses under physiological conditions with maintained bile acid homeostasis. In summary, our findings suggest that taurine-conjugated bile acids in both plasma and liver, particularly TCA, can serve as early and sensitive markers for predicting intrahepatic cholestatic drugs and can act as potent exacerbators of cholestatic liver injury progression. However, exogenous TCA does not induce liver injury under physiological conditions where bile acid homeostasis is maintained.

A genome-wide investigation of the mechanism underlying the effect of exogenous boron application on sugar content and overall quality of “Benihoppe” strawberries

In recent years, the widespread application of growth regulators and nutrients to boost yield and quality of strawberry fruits has led to the rapid growth of strawberry industry globally. Although the effects of major nutrients on strawberry yield have been widely studied, investigations into the effect of trace elements such as boron remain limited. This study examined the effect of boron application on the yield and quality of “Benihoppe” strawberry fruits. Nutrient solutions with varying boron concentrations (0, 0.024, 0.048, 0.072, and 0.096 mM) were applied to the plants, and their effect on fruit quality was evaluated. The results indicated that boron application enhanced the yield per plant, nutrient composition (total amino acid and vitamin C content), antioxidant properties (total phenol) and volatile components (esters) in strawberry fruits. Specifically, treatment with 0.048 mM boron concentration significantly increased the accumulation of soluble sugars, such as sucrose, whose concentration was 154.29% higher than that of the control treated with 0 mM concentration. This enhancement is attributable to the regulated expression of sucrose phosphate synthase (maker-Fvb2-2-augustus-gene-229.38) and β-fructofuranosidase-1/2/3 (augustus-masked-Fvb5-4-processed-gene-2.0, maker-Fvb5-3-augustus-gene-272.30, and maker-Fvb5-1-augustus-gene-0.37) genes, which play crucial roles in sugar metabolism and enzyme activity. Overall, boron application enhanced the quality of “Benihoppe” strawberries. The findings of this study offer substantial theoretical and practical guidance for using boron fertilizers in strawberry farming.

Hyperglycosylation impairs the inhibitory activity of rCdtPLI2, the first recombinant beta-phospholipase A2 inhibitor

Crotoxin, a phospholipase A2 (PLA2) complex and the major Crotalus venom component, is responsible for the main symptoms described in crotalic snakebite envenomings and a key target for PLA2 inhibitors (PLIs). PLIs comprise the alpha, beta and gamma families, and, due to a lack of reports on beta-PLIs, this study aimed to heterologously express CdtPLI2 from Crotalus durissus terrificus venom gland to improve the knowledge of the neglected beta-PLI family. Thereby, recombinant CdtPLI2 (rCdtPLI2) was produced in the eukaryotic Pichia pastoris system to keep some native post-translational modifications. rCdtPLI2 (~41 kDa) presents both N- and O-linked glycans. Alpha-mannosidase digested-rCdtPLI2 (1 mol) strongly inhibited (73 %) CB-Cdc catalytic activity (5 mol), demonstrating that glycosylations performed by P. pastoris affect rCdtPLI2 action. Digested-rCdtPLI2 also inhibited PLA2s from diverse Brazilian snake venoms. Furthermore, rCdtPLI2 (1 mol) abolished the catalytic activity of Lmr-PLA2 (5 mol) and reduced the CTx-Cdc (5 mol) enzyme activity by 65 %, suppressing basic and acidic snake venom PLA2s. Additionally, crotalic antivenom did not recognize rCdtPLI2, suggesting a lack of neutralization by antivenom antibodies. These findings demonstrate that studying snake venom components may reveal interesting novel molecules to be studied in the snakebite treatment and help to understand these underexplored inhibitors.

Copper sulfate-induced stress in Spinach: Metabolic pathway disruption and plant response

Copper sulfate (CuSO4) stress profoundly affects plant growth by interfering with key metabolic pathways. This disruption leads to significant alterations in various physiological parameters, ultimately impacting the overall health and productivity of the plant. This study assessed the impact of CuSO4 stress on spinach (Spinacia oleracea L.) through a pot experiment using CuSO4 concentrations of 0, 75, 125, and 175 ppm. We noticed that at 75 ppm, CuSO4 improved plant height and the concentration of soluble sugar and ascorbic acid compared to the control. Additionally, amino acid, phenol, proline, fresh weight, and moisture content peaked at 175 ppm. Conversely, at 125 and 175 ppm, plant height, dry weight, leaf area, and concentrations of ascorbic acid and sugar significantly decreased. Moreover, at 175 ppm, there were substantial decreases in chlorophyll a (14.8%), chlorophyll b (73.6%), carotenoids (15%), and photosynthetic rates compared to the control. However, the chlorophyll a to chlorophyll b ratio increased by 29.53% at 175 ppm. In addition, protein and phenol contents diminished at 75 and 125 ppm. Elevated CuSO4 levels increased non-protein thiol levels while reducing the activities of superoxide dismutase, catalase, ascorbate peroxidase, and glutathione peroxidase. Stress hormones such as abscisic acid, jasmonic acid, and ethylene increased with CuSO4 stress, whereas growth hormones indol-acetic acid and gibberellic acid declined. This study demonstrates that spinach shows improved growth and metabolic function at 75 ppm CuSO4, indicating tolerance to mild stress. However, higher CuSO4 concentrations (125 and 175 ppm) significantly reduce growth parameters, chlorophyll content, and enzyme activities, highlighting the need for careful CuSO4 management in agriculture to avoid adverse effects on plant health and productivity.

Potencial bioindicador de mudas de Cedrela fissilis em áreas contaminadas por cobre

ABSTRACT Soil contamination with toxic metals brings along severe environmental issues. Among these metals, copper (Cu) is harmful to plant development when it reaches high contamination levels in the soil. Thus, identifying species capable of resisting this contamination type helps these sites’ revegetation and decontamination processes. Therefore, the present study aimed to investigate the tolerance of Cedrela fissilis plants to excess Cu through morphophysiological and biochemical variables. C. fissilis seedlings were subjected to five concentrations of Cu (0, 2, 4, 6, and 8 mg L-1). The experimental design was completely randomized, with five treatments and four repetitions. Morphophysiological (number of leaves, shoot height, root length, dry weight, morphological variables of the root system, and leaf area) and biochemical (antioxidant enzymes, lipid peroxidation, hydrogen peroxide concentration, and photosynthetic pigments) traits and Cu accumulated in roots and shoot were evaluated. High concentrations of Cu had a negative effect on the shoot and root dry weight, photosynthetic rate, stomatal conductance, and transpiration rate. Overall, Cu increased the activity of the antioxidant enzymes and lipid peroxidation. Therefore, Cu incidence in the nutrient solution has negatively influenced the biochemical and physiological traits of C. fissilis seedlings to the detriment of their growth. Thus, it was possible to identify sensitive behavior by the investigated species. Because of these features, C. fissilis seedlings can be used as markers for copper-contaminated areas.

Evaluating the Protective Effect of Melatonin on Atorvastatin-induced Mitochondrial Toxicity in Pancreatic Beta Cells.

Atorvastatin and other statins belong to a category of cholesterollowering drugs, which may cause some damage to pancreatic cells despite their effectiveness. The present study investigated the effects of melatonin against atorvastatin-induced toxicity on islets of Langerhans and CRI-D2 cells. The MTT assay was used to determine cell viability. The effect of various concentrations of melatonin (0,10, 50, 100, 250, 500 and 1000 μM) on CRI-D2 cell viability was evaluated for 24 hours to determine the non-cytotoxic concentrations of melatonin. Additionally, cells were treated with different concentrations of atorvastatin (10, 100, and 150 ng/mL) for 24 hours to determine a concentration that could induce the maximum cell death. After selecting the appropriate concentrations for melatonin, cells were treated with atorvastatin (10, 100, and 150 ng/ml) and melatonin (10 and 100 μM) simultaneously for a period of 24 hours. Malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase, catalase, and glutathione peroxidase activity were assessed as indicators of oxidative stress. To assess mitochondrial function, the ratio of adenosine diphosphate (ADP) to adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP) were measured. Atorvastatin markedly raised ROS and MDA levels. This result was associated with a decrease in MMP, an increase in the ADP/ATP ratio, and a change in the activity of antioxidant enzymes. Atorvastatin (150 ng/mL)-induced mitochondrial damage was alleviated by concurrent melatonin and atorvastatin therapy. These results suggest that melatonin has a protective effect against atorvastatininduced toxicity in the mitochondria of pancreatic cells.

Decoding the role of HIF-1α in immunoregulation in Litopenaeus vannamei under hypoxic stress

Hypoxia poses a significant challenge to aquatic organisms, especially Litopenaeus vannamei (L. vannamei), which play a vital role in the global aquaculture industry. Hypoxia-inducible factor 1α (HIF-1α) is a pivotal regulator of the organism's adaptation to hypoxic conditions. To understand of how HIF-1α affects the immunity of L. vannamei under hypoxic conditions, we conducted a thorough study involving various approaches. These included observing tissue morphology, analyzing the expression of immune-related genes, assessing the activities of immune-related enzymes, and exploring immune-related pathways. Our study revealed that RNA interference (RNAi)-mediated knockdown of HIF-1α markedly reduced HIF-1α expression in the gill (75 to 95%), whereas the reduction ranged from 2 to 43% in the hepatopancreas. Knockdown of HIF-1α resulted in increased damage to both gill and hepatopancreatic tissues in hypoxic conditions. Additionally, immune-related genes, including Astakine (AST), Hemocyanin (HC), and Ferritin (FT), as well as immune-related enzymes such as Acid Phosphatase (ACP), Alkaline Phosphatase (AKP), and Phenoloxidase (PO), exhibited intricate regulatory patterns in response to hypoxia stress following the knockdown of HIF-1α. Transcriptome analysis revealed that HIF-1α knockdown significantly impacts multiple signaling pathways, including the JAK-STAT signaling pathway, Th17 cell differentiation pathways, PI3K-Akt signaling pathway, ErbB signaling pathway, MAPK signaling pathway, chemokine signaling pathway, ribosomal pathways, apoptosis, lysosomes and arachidonic acid metabolism. These alterations disrupt the organism's immune balance and interfere with normal metabolic processes, potentially leading to various immune-related diseases. We speculate that the weakened immune response resulting from HIF-1 inhibition is due to the reduced metabolic capacity, and the existence of a direct regulatory relationship between them requires further exploration. This study greatly advances our understanding of the vital role that HIF-1α plays in regulating immune responses in shrimp under hypoxic conditions, thereby deepening our comprehension of this critical biological mechanism.

Trivalent chromium stress trigger accumulation of secondary metabolites in rice plants: Integration of biochemical and transcriptomic analysis

Trivalent chromium [Cr (III)] is a frequently detected environmental contaminant that negatively affects plant metabolism, growth, and yield. Plant secondary metabolites are non-nutrient compounds involved in diverse physiological functions in response to abiotic stresses. This study performed biochemical and transcriptomic analyses to clarify the protective role and mechanism of secondary metabolites in rice seedlings under Cr(III) stress. The content of measured secondary metabolites i.e., total soluble phenolics, flavonoids, lignin, and anthocyanin in rice tissues was significantly enhanced under Cr(III) exposure. Additionally, the activities of several enzymes including chalcone synthase, phenylalanine ammonialyase, peroxidase, and anthocyanidin synthase, were positively activated. Transcriptomic analysis revealed a number of differentially expressed genes (DEGs) in Cr(III)-treated rice seedlings and their expression patterns are tissue-specific. Additionally, the DEGs involved in secondary metabolism pathways were evident after KEGG enrichment analysis. Cr(III) exposure resulted in distinct genetic regulation strategies in rice tissues, with different DEGs activating various sub-pathways in the secondary metabolism pathways to cope with Cr(III) stress. Furthermore, the integrated correlation analysis of the secondary metabolites and transcriptome data identified key genes involved in different steps of the sub-pathways of secondary metabolism pathway in rice plants under Cr(III) stress. This study indicates that the accumulation of secondary metabolites in rice plants is a survival and detoxification strategy to reduce the adverse effects of toxic compounds. Future research should explore how key genes in secondary metabolism pathways aid in Cr(III) detoxification and enhance crop stress tolerance.

Structural changes of potato starch and activity inhibition of starch digestive enzymes by anthocyanin from lingonberry (Vaccinium uliginosum L.) retarded starch digestibility

The effects of anthocyanins on in vitro and in vivo digestibility of potato starch were evaluated in this study. Then the influence of anthocyanins on physicochemical property of potato starch and the activity of starch digestive enzymes (α-amylase and α-glucosidase) were also investigated to understand the mechanism of anthocyanins on starch digestibility. Results have shown that dietary anthocyanins could effectively inhibit the biological activities of α-amylase and α-glucosidase to delay the peak of postprandial blood glucose. Characterization of physicochemical properties of potato starch indicates a structural change due to the presence of anthocyanins, hindering its access to starch digestive enzymes. Among all anthocyanins, lingonberry anthocyanin significantly promoted the retrogradation of potato starch (7.153 % to 25.913 %) and exert promising inhibition on α-amylase and α-glucosidase. Lingonberry anthocyanins mainly interacted with potato starch through hydrogen bonds, which reduce the amount of amylose molecules leached from potato starch and loosen the three-dimensional (3D) network structure of starch gel. This study could provide theoretical evidence for utilization of anthocyanins in diabetic-management function food.

Insights into multivalent metal removal-assistant anaerobic fermentation of waste activated sludge: Impact factor identification and mechanism clarification of metal removal

The study investigated the impact factors of metal removal and their role in enhancing anaerobic fermentation of waste activated sludge (WAS), aiming to identify key mechanisms. By optimizing the sludge concentration, it found that a sludge suspension solid range of 10–30 g/L significantly improved the efficiency of anaerobic fermentation, and yielded SCOD of 93.8–177.1 mg/g volatile suspension solid after 8 h, respectively, which was 3.67–4.77 times higher than the control. Correspondingly, the production of short-chain fatty acids (SCFAs) was significantly enhanced. At the optimal sludge suspension solid of 10–30 g/L, the SCFAs were 1.28–1.51 times higher than that of the control. Furthermore, the study evaluated the performance of different metal removal reagents and discovered that microporous COOH reagent outperformed gel SO3H and macroporous SO3H reagent. The macroporous COOH reagent achieved 1.54 and 1.22 times higher SCOD values and significantly enhanced the production of SCFAs, demonstrating its superiority in metal removal and fermentation enhancement. Moreover, the research revealed that sludge concentration and metal removal agent types influenced the activities of key enzymes involved in anaerobic fermentation. Additionally, the macroporous COOH reagent showed the most efficient ability to remove metal ions, contributing to increased nutrient recovery in terms of nitrogen (NH4+-N) and total phosphorus (TP) release during the acidification process. In summary, the enhancing mechanism of metal removal-assistant anaerobic fermentation was discussed from the sludge floc concentration, the skeleton structure and the ion exchange group type. The identified mechanism significantly improves fermentation efficiency and facilitate the organic recovery, representing an innovative approach for wide application in WAS management and resource recovery.

Probiotics by Modulating Gut-Brain Axis Together With Brivaracetam Mitigate Seizure Progression, Behavioral Incongruities, and Prevented Neurodegeneration in Pentylenetetrazole-Kindled Mice.

The microbiota-gut-brain axis (MGBA) is a central nexus that integrates higher cognitive and emotional centers of the central nervous system (CNS) within the intricate functioning of the intestine. Accumulating evidence suggests that dysbiosis in the taxonomic diversity of gut flora plays a salient role in the progression of epilepsy and comorbid secondary complications. In the current study, we investigated the impact of long-term oral bacteriotherapy (probiotics; 10 mL/kg; 109 colony-forming unit/ml) as an adjunctive treatment intervention with brivaracetam (BRV; 10 mg/kg) over 21 days on pentylenetetrazole (PTZ) induced augmented epileptic response and associated electrographical and behavioral perturbations in mice. Moreover, we also unveiled antioxidant capacity and histopathologic changes in treated versus non-treated animals. Results revealed combination increases seizure threshold and prevented high ictal spiking. Additionally, it alleviated PTZ-induced neuropsychiatric disturbances such as anxiety and depressive-like phenotype along with cognitive deficits. Furthermore, dual therapy prompted physiological oxidant/antioxidant balance as evidenced by increased activity of antioxidant enzymes (SOD and catalase) and reduced levels of oxidative stressor (MDA). This therapeutic intervention with commensal species suppressed network-driven neuroinflammation and preserved normal cytoarchitecture with intact morphology in the pyramidal layers of cornu ammonis (CA1 and CA3). Our study provides supporting evidence for the use of probiotics as adjunctive therapy with anti-seizure medications to modulate epileptogenic processes and related multimorbidities, particularly in individuals with drug-resistant seizures.