G6PDH Activity Research Articles

Influence of Water and Fertilizer Reduction on Respiratory Metabolism in Sugar Beet Taproot (Beta vulgaris L.).

Inner Mongolia, a major region in China for growing sugar beet, faces challenges caused by unscientific water and fertilizer management. This mismanagement restricts the improvement of sugar beet yield and quality and exacerbates water waste and environmental pollution. This study aims to evaluate the effects of reduced water and fertilizer on the growth and physiological metabolism of sugar beet taproot. Field experiments were conducted in Ulanqab, Inner Mongolia, in 2022 and 2023, using a split-plot design with three levels each of fertilization and irrigation. The study analyzed the effects of reduced water and fertilizer treatments on fresh taproot weight, respiration rate, energy metabolism, respiratory enzyme activity, and gene expression in sugar beet taproot. It was found that a 10% reduction in fertilizer significantly increased the beet taproot fresh weight. Further research revealed that during the rapid leaf growth phase and the taproot and sugar growth period, a 10% reduction in fertilizer upregulated HK and IDH gene expression and downregulated G6PDH gene expression in the beet taproot. This increased HK and IDH activities, decreased G6PDH activity, enhanced the activity of the EMP-TCA pathway, and inhibited the PPP. Taproot weight was positively correlated with the respiration rate, ATP content, EC, and ATPase, HK, and IDH activities, thereby increasing the taproot growth rate and taproot fresh weight, with an average increase of 4.0% over two years. These findings introduce a novel method for optimizing fertilizer use, particularly beneficial in water-scarce regions. Implementing this strategy could help farmers in western Inner Mongolia and similar areas improve crop yield and sustainability. This study offers new insights into resource-efficient agricultural practices, highlighting the importance of customized fertilization strategies tailored to local environmental conditions.

L-arginine combination with 5-fluorouracil inhibit hepatocellular carcinoma cells through suppressing iNOS/NO/AKT-mediated glycolysis.

L-arginine can produce nitric oxide (NO) under the action of inducible nitric oxide synthase (iNOS), while 5-fluorouracil (5-FU) can induce the increase of iNOS expression. The present study was to investigate the mechanism of L-arginine combined with 5-FU regulating glucose metabolism of hepatocellular carcinoma (HCC) through iNOS/NO/AKT pathway. The combination of L-arginine and 5-FU resulted in decreased cell survival and exhibited synergistic cytotoxic effects in HepG2 and SMMC7721 cells. Meanwhile, L-arginine increased 5-FU inhibitory effect on HepG2 and SMMC7721 cells by increasing NO production. Co-treatment with L-arginine and 5-FU resulted in a significant decrease in both G6PDH and LDH enzymatic activities, as well as reduced levels of ATP and LD compared to treatment with L-arginine or 5-FU alone. Moreover, the combination of L-arginine and 5-FU resulted in a decrease in the expression of GLUT1, PKM2, LDHA, p-PI3K and p-AKT. Furthermore, the combination demonstrated a synergistic effect in downregulating the expression of HIF-1α and β-catenin, which were further diminished upon the addition of shikonin, a specific inhibitor of PKM2. LY294002 treatment further reduced the expression of GLUT1, PKM2, and LDHA proteins induced by combined L-arginine and 5-FU treatment compared to the combined group. However, the reduction in p-PI3K, p-AKT, and GLUT1 expression caused by L-arginine and 5-FU combination was also reversed in HepG2 and SMMC7721 cells with iNOS knockdown, respectively. Additionally, the combination of L-arginine and 5-FU led to a greater reduction in the enzymatic activity of ALT, AST, G6PDH and LDH, as well as a significant reduction in hepatic index, AFP, AFP-L3, ATP and LD levels in a rat model of HCC. Moreover, the simultaneous administration of L-arginine and 5-FU significantly improved the gross morphology of the liver, reduced nuclear atypia, inhibited the proliferation of cancer cells, and decreased the expression levels of p-PI3K, p-AKT, GLUT1, PKM2, and LDHA, while iNOS expression was increased in the combination group. Taking together, L-arginine and 5-FU combination resulted in the inhibition of enzymes in aerobic glycolysis via the iNOS/NO/AKT pathway, which led to the suppression of glucose metabolism and downregulation of nuclear transcription factors, thereby impeding the proliferation of hepatocellular carcinoma cells.

Cannabinoids induce cell death in leukaemic cells through Parthanatos and PARP-related metabolic disruptions

BackgroundSeveral studies have described a potential anti-tumour effect of cannabinoids (CNB). CNB receptor 2 (CB2) is mostly present in hematopoietic stem cells (HSC). The present study evaluates the anti-leukaemic effect of CNB.MethodsCell lines and primary cells from acute myeloid leukaemia (AML) patients were used and the effect of the CNB derivative WIN-55 was evaluated in vitro, ex vivo and in vivo.ResultsWe demonstrate a potent antileukemic effect of WIN-55 which is abolished with CB antagonists. WIN-treated mice, xenografted with AML cells, had better survival as compared to vehicle or cytarabine. DNA damage-related genes were affected upon exposure to WIN. Co-incubation with the PARP inhibitor Olaparib prevented WIN-induced cell death, suggesting PARP-mediated apoptosis which was further confirmed with the translocation of AIF to the nucleus observed in WIN-treated cells. Nicotinamide prevented WIN-related apoptosis, indicating NAD+ depletion. Finally, WIN altered glycolytic enzymes levels as well as the activity of G6PDH. These effects are reversed through PARP1 inhibition.ConclusionsWIN-55 exerts an antileukemic effect through Parthanatos, leading to translocation of AIF to the nucleus and depletion of NAD+, which are reversed through PARP1 inhibition. It also induces metabolic disruptions. These effects are not observed in normal HSC.

DHEA down-regulates mitochondrial dynamics and promotes apoptosis of lung adenocarcinoma cells through FASTKD2.

Background: DHEA is a steroid hormone produced by the gonads, adrenal cortex, brain, and gastrointestinal tract. While the anti-obesity, anti-atherosclerosis, anti-cancer, and memory-enhancing effects of DHEA have been substantiated through cell experiments, animal studies, and human trials, the precise mechanisms underlying these effects remain unclear. Altered mitochondrial dynamics can lead to mitochondrial dysfunction, which is closely related to many human diseases, especially cancer and aging. This study was to investigate whether DHEA inhibits lung adenocarcinoma through the mitochondrial pathway and its molecular mechanism. Methods: Through animal experiments and cell experiments, the effect of DHEA on tumor inhibition was determined. The correlation between FASTKD2 expression and DHEA was analyzed by Western blot, Reverse transcription-quantitative PCR, Immunohistochemistry, and TCGA database. Results: In this study, DHEA supplementation in the diet can inhibit the tumor size of mice, and the effect of adding DHEA one week before the experiment is the best. DHEA limits the glycolysis process by inhibiting G6PDH activity, increases the accumulation of reactive oxygen species, and initiates apoptosis in the mitochondrial pathway of cancer cells. Conclusion: DHEA suppresses mitochondrial fission and promotes mitochondrial fusion by downregulating the expression of FASTKD2, thereby inhibiting tumor growth and prolonging the overall survival of lung adenocarcinoma patients, which also provides a new target for the prevention and treatment of lung adenocarcinoma.

FoxO3a Drives the Metabolic Reprogramming in Tamoxifen-Resistant Breast Cancer Cells Restoring Tamoxifen Sensitivity.

Tamoxifen-resistant breast cancer cells (TamR-BCCs) are characterized by an enhanced metabolic phenotype compared to tamoxifen-sensitive cells. FoxO3a is an important modulator of cell metabolism, and its deregulation has been involved in the acquisition of tamoxifen resistance. Therefore, tetracycline-inducible FoxO3a was overexpressed in TamR-BCCs (TamR/TetOn-AAA), which, together with their control cell line (TamR/TetOn-V), were subjected to seahorse metabolic assays and proteomic analysis. FoxO3a was able to counteract the increased oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) observed in TamR by reducing their energetic activity and glycolytic rate. FoxO3a caused glucose accumulation, very likely by reducing LDH activity and mitigated TamR biosynthetic needs by reducing G6PDH activity and hindering NADPH production via the pentose phosphate pathway (PPP). Proteomic analysis revealed a FoxO3a-dependent marked decrease in the expression of LDH as well as of several enzymes involved in carbohydrate metabolism (e.g., Aldolase A, LDHA and phosphofructokinase) and the analysis of cBioPortal datasets of BC patients evidenced a significant inverse correlation of these proteins and FoxO3a. Interestingly, FoxO3a also increased mitochondrial biogenesis despite reducing mitochondrial functionality by triggering ROS production. Based on these findings, FoxO3a inducing/activating drugs could represent promising tools to be exploited in the management of patients who are refractory to antiestrogen therapy.

Inhibitory effect and mechanism of action of blue light irradiation on adipogenesis

Blue light can reach the epidermis, dermis, and hypodermis of the skin and affect the physiology of each cell type. However, thus far, most studies have focused on the effects of blue light on the epidermis and dermis; no studies have been conducted on the effects of blue light on the hypodermis. In this study, we attempted to elucidate the effects of blue light on the hypodermis. Specifically, we investigated the effects of blue light on 3T3-L1 adipogenesis and its mechanism of action. In this study, we found that blue light reduced lipid accumulation and GPDH activity, indicating its antiadipogenic properties. Furthermore, blue light inhibited the mRNA and protein levels of peroxisome proliferator-activated receptor γ (PPARγ) and its target genes, such as Fasn and FABP4, and the luciferase activity of the PPRE promoter, suggesting that blue light downregulates the expression of adipogenic genes, leading to suppression of 3T3-L1 adipogenesis. Furthermore, blue light increased the phosphorylation of PPARγ, indicating its anti-adipogenic effect through PPARγ degradation. Blue light upregulates the expression and phosphorylation of transient receptor potential vanilloid 1 (TRPV1). Furthermore, blue light restored calcium influx, which was attenuated by adipogenesis. These data suggest that TRPV1 is involved in the anti-adipogenic effects of blue light. Blue light induced the phosphorylation of AMPK, ACC, and MAPKs, whereas capsazepine, an antagonist of TRPV1, attenuated the effects of blue light. Capsazepine treatment also reduced the blue light-induced anti-adipogenic effects. These results indicate that TRPV1 operates upstream of AMPK or MAPKs in the blue light-induced anti-adipogenesis process, which is mediated by activating the TRPV1-AMPK/MAPK signaling pathways. Meanwhile, inhibition of AMPK and MAPKs reduced the phosphorylation level of PPARγ, indicating that AMPK/MAPK signaling contributes to the phosphorylation of PPARγ. These results suggest the possibility of using blue light as an antiadipogenic agent.

Ameliorative Effect of Ginger on Blood Glucose Levels and Cardiac TCA Cycle Enzymes Activity in STZ Induced Diabetic Rat

This study aimed to investigate the effects of ginger administration on altered blood glucose levels, cytosolic and mitochondrial enzymes (TCA cycle enzymes) activity in streptozotocin-induced diabetes rats. The study divided Wistar strain rats into five groups: normal control, ginger treated, diabetic control, diabetic plus ginger treated, and diabetic plus glibenclamide treated groups. The diabetic group had significantly elevated blood glucose levels, which were significantly lowered by ginger administration. The cytosolic enzyme G6PDH activity was significantly (P<0.001) decreased along with a significant increase in the LDH activity in diabetic rats heart tissue. The activities of SDH, MDH, GDH in the heart tissue of diabetic rats were significantly decreased, but the daily oral treatment of ginger to diabetic rats for thirty days reversed the above changes in a significant (P<0.001) manner. The study demonstrated that an ethanolic extract of ginger could lower blood glucose levels, improve enzyme activities and body weight in diabetic rats. This suggests that ginger extracts could be used as a cardio-protective supplement to reverse diabetic-induced complications.

LDH-A Promotes Metabolic Rewiring in Leucocytes from the Intestine of Rats Treated with TNBS.

Although the aetiology of inflammatory bowel diseases (IBDs) is still unknown, one of their main characteristics is that the immune system chronically affects the permeability of the intestinal lamina propria, in turn altering the composition of the microbiota. In this study, the TNBS rat model of colitis was used because it contains a complex inflammatory milieu of polymorphonuclear cells (PMN) and lymphocytes infiltrating the lamina propria. The aim of the present study was to investigate six dehydrogenases and their respective adaptations in the tissue microenvironment by quantifying enzymatic activities measured under substrate saturation conditions in epithelial cells and leukocytes from the lamina propria of rats exposed to TNBS. Our results show that in the TNBS group, an increased DAI score was observed due to the presence of haemorrhagic and necrotic areas in the colon. In addition, the activities of G6PDH and GADH enzymes were significantly decreased in the epithelium in contrast to the increased activity of these enzymes and increased lactate mediated by the LDH-A enzyme in leukocytes in the lamina propria of the colon. Over the past years, evidence has emerged illustrating how metabolism supports aspect of cellular function and how a metabolic reprogramming can drive cell differentiation and fate. Our findings show a metabolic reprogramming in colonic lamina propria leukocytes that could be supported by increased superoxide anion.

Prepubertal oral exposure to relevant doses of acrylamide impairs the testicular antioxidant system in adulthood, increasing protein carbonylation and lipid peroxidation

The increased prevalence of human infertility due to male reproductive disorders has been linked to extensive exposure to chemical endocrine disruptors. Acrylamide (AA) is a compound formed spontaneously during the thermal processing of some foods that are mainly consumed by children and adolescents. We previously found that prepubertal exposure to AA causes reduced sperm production and functionality. Oxidative stress is recognized as the main cause of reduced sperm quality and quantity. In this sense, our objective was to evaluate the expression and activity of genes related to enzymatic antioxidant defense, nonprotein thiols, lipid peroxidation (LPO), protein carbonylation (PC) and DNA damage in the testes of rats exposed to acrylamide (2.5 or 5 mg/kg) from weaning to adult life by gavage. For the AA2.5 and AA5 groups, there were no alterations in the transcript expression of genes related to enzymatic antioxidant defense. The enzymatic activities and metabolic parameters were also not affected in the AA2.5 group. For the AA5 group, the enzymatic activities of G6PDH and GPX were reduced, SOD was increased, and protein carbonylation (PC) was increased. Data were also evaluated by Integrate Biomarker Response (IBRv2), a method to analyze and summarize the effects on biomarkers between doses. The IBRv2 index was calculated as 8.9 and 18.71 for AA2.5 and AA5, respectively. The following biomarkers were affected by AA2.5: decreased enzymatic activities of G6PDH, SOD, and GPX, increased GST and GSH, increased LPO and PC, and decreased DNA damage. For AA5, decreased enzymatic activities of G6PDH, GST, CAT and GPX, increased SOD and GSH, increased PC, and decreased LPO and DNA damage were observed. In conclusion, AA exposure during the prepubertal period causes imbalances in the testicular enzymatic antioxidant defense, contributing to the altered spermatic scenario in the testes of these rats.

Downregulation of ferredoxin-NADP+ oxidoreductase enhances oxidized pentose phosphate pathway via NADPH/NADP+ ratio in the strong resurrection intertidal red alga Neopyropia yezoensis with economic value

Ferredoxin-NADP+ oxidoreductase (FNR) is involved in reducing Fd in linear electron transportation (LET) in chloroplast. While the oxidized pentose phosphate pathway (OPPP) occurred in cytoplasm has close relationship with cyclic electron transportation (CET) under stress condition. However, whether FNR and OPPP cooperate with each other, and in what way they are associated remains unclear. In this study, Neopyropia yezoensis, a strong resurrection red macroalga, was used to study the relationship between FNR and OPPP. FNR genetic transformation strains of N. yezoensis, fnrOE (overexpression) and fnrSi (silence) were obtained. The results showed that the growth rate of fnrSi was reduced remarkably. The expression level of genes encoding key enzymes in OPPP and enzyme activity of G6PDH were up regulated in transgenic strains, indicating the enhancement of OPPP. Besides, the NADPH and NADP+ content in WT and transgenic lines were also measured. Y (I) of both fnrOE and fnrSi decreased significantly under dark treatment, indicating that FNR content synergistically affected CET pathway with OPPP in N. yezoensis. All the results indicated that changes of FNR content could enhance OPPP, which further promote the CET operation. This is the first time to find the close relationship between photosynthetic electron transportation and carbohydrate metabolism in strong resurrection plant.

Toxic copper level increases erythrocyte glycolytic rate, glutathione production and alters electrolyte balance in male Wistar rats

BackgroundCopper is a micronutrient vital to several cellular energy metabolic processes and drives erythropoiesis. However, it disrupts cellular biological activities and causes oxidative damage when in excess of cellular needs. This study investigated the effects of copper toxicity on erythrocyte energy metabolism in male Wistar rats. MethodsTen Wistar rats (150–170 g) were randomly divided into 2 groups: control (given 0.1 ml distilled water) and copper toxic (given 100 mg/kg copper sulphate). Rats were orally treated for 30 days. Blood, collected retro-orbitally after sodium thiopentone anaesthesia (50 mg/kg i.p.) into fluoride oxalate and EDTA bottles, was subjected to blood lactate assay and extraction of red blood cell respectively. Red blood cell nitric oxide (RBC NO), glutathione (RBC GSH), adenosine triphosphate (RBC ATP) levels, RBC hexokinase, glucose-6-phosphate (RBC G6P), glucose-6-phosphate dehydrogenase (RBC G6PDH), and lactate dehydrogenase (RBC LDH) activity was estimated spectrophotometrically. Values (Mean±SEM, n = 5) were compared by Student’s unpaired T-test at p < 0.05. Results and conclusionCopper toxicity significantly increased RBC hexokinase (23.41 ± 2.80 µM), G6P (0.48 ± 0.03 µM), G6PDH (71.03 ± 4.76nmol/min/ml) activities, ATP (624.70 ± 57.36 µmol/gHb) and GSH (3.08 ± 0.37 µM) level compared to control (15.28 ± 1.37 µM, 0.35 ± 0.02 µM, 330.30 ± 49.58 µmol/gHb, 54.41 ± 3.01nmol/min/ml and 2.05 ± 0.14 µM respectively, p < 0.05). Also, RBC LDH activity (145.00 ± 19.88mU/ml), NO (3.45 ± 0.25 µM) and blood lactate (31.64 ± 0.91 mg/dl) level were lowered significantly compared to control (467.90 ± 94.23mU/ml, 4.48 ± 0.18 µM and 36.12 ± 1.06 mg/dl respectively). This study shows that copper toxicity increases erythrocyte glycolytic rate and glutathione production. This increase could be connected to a compensatory mechanism for cellular hypoxia and increased free radical generation.

Comparative biochemical and molecular responses of biotransformation and antioxidant systems in three species of Crassostrea (Sacco, 1897) oysters exposed to chrysene

Chrysene (CHR) is among the most persistent polycyclic aromatic hydrocarbons (PAH) in water and a priority compound for pollutants monitoring, due to its carcinogenic, mutagenic and genotoxic potential. Aquatic animals exposed to CHR may present alterations of biomarkers involved in the biotransformation and oxidative stress-related parameters. The aim of this study was to investigate differences in antioxidant and biotransformation (phase I and II) systems of Crassostrea gigas, C. gasar and C. rhizophorae and its effects resulting from CHR exposure. Adult oysters of these species were exposed to 10 μg L−1 of CHR for 24 h and 96 h. In gills, the transcripts CYP1-like, CYP2-like, CYP2AU1-like, GSTO-like, MGST-like, SULT-like were evaluated after 24 h of exposure. The activity of SOD, CAT, GPx, GR and G6PDH were analyzed in gills and digestive glands after 96 h of exposure. CHR bioaccumulated in tissues. Differences in the remaining levels of CHR in water after 96 h were observed in aquaria containing C. gigas or C. gasar oysters and may be associated to the different filtration rates between these species. Downregulate of biotransformation genes were observed in gills of C. gasar (CYP2AU1-like and GSTO-like) and C. rhizophorae (CYP1-like1, CYP2-like, MGST-like and SULT-like), suggesting that biotransformation responses may be species-specific. Differential activity of antioxidant enzymes were observed in gills and digestive gland of oysters exposed to CHR. Biochemical responses suggested that C. gigas and C. gasar are more responsive to CHR. Differential responses observed among the three Crassostrea species can be related to evolutionary differences, ecological niches and adaptation to environment.

Growth Performance, Digestive Enzyme Activities, and Oxidative Stress Markers in the Proximal Intestine of European Sea Bass (Dicentrarchus labrax) Fed High Starch or Lipid Diets

The effect of different main dietary compositions on growth, anticipatory digestive enzyme activities, and oxidative status was studied in the proximal intestine of juvenile European sea bass. A control diet (C, 44% protein, 17.6% lipid, and 20% starch), three diets with increasing starch levels to test protein sparing (P36S36, P40S29, and P43S24), and two diets with high lipid content (L20S13 and L22S7) were tested. After 20 weeks, growth, digestive enzyme activities, lipid peroxidation, antioxidant enzyme activities, and G6PDH activity were measured after a 24-h fast. Sea bass fed P43S24 and L20S13 maintained an oxidative status like C fish, up-regulated CAT activity, and adjusted anticipatory protease activity. Instead, the lipid peroxidation increased in the L22S7 group, although CAT activity increased, whereas anticipatory total protease activity was downregulated. P40S29 also triggered LPO and CAT activity, but G6PDH levels diminished significantly. Moreover, an up-regulation in digestive enzyme activities was found. Finally, P36S36 fish showed less antioxidant enzyme activity and G6PDH, although their LPO tended to increase and their lipase and α-amylase activities were upregulated. In conclusion, the inclusion of carbohydrates up to 24% or lipids up to 20% is possible for this species if protein requirements are met without negative effects on growth.

Oxidative status of Ctenomys flamarioni (Rodentia: Ctenomyidae) in natural areas with different levels of anthropic activity in southern Brazil

Rampant urbanization in coastal environments turns areas close to the seafront into a highly impacted ecosystem, possibly affecting the health and well-being of resident animal species. The tuco-tuco Ctenomys flamarioni is an endemic and endangered subterranean mammal from southern Brazil, and the anthropic influence was considered one of the main threats to the species. In this context, the present study aimed to investigate the patterns of oxidative status of the species in natural areas with different levels of anthropogenic disturbance. We evaluated two populations of C. flamarioni, one located in an area with intense anthropogenic impact due to urbanization and tourist activity, and the other in a non-impacted area. Oxidative injury parameters (lipid peroxidation and carbonylated protein levels), and the activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, glucose 6-phosphate dehydrogenase, glutathione S-transferase and carboxylesterase were measured. Individuals inhabiting the impacted area had lower G6PDH activity and higher levels of carbonylated proteins. This combination of higher level of oxidative damage and lower antioxidant activity is an indication that the oxidative status of animals in the impacted population is possibly being affected as a consequence of anthropogenic activities in this environment. The values of the parameters obtained in the current study can be used as a reference of the oxidative state of C. flamarioni in future studies with tuco-tucos.

Oral Administration of Chaetoceros gracilis—A Marine Microalga—Alleviates Hepatic Lipid Accumulation in Rats Fed a High-Sucrose and Cholesterol-Containing Diet

Microalgae are attracting attention as a next-generation alternative source of protein and essential fatty acids that do not consume large amounts of water or land. Chaetoceros gracilis (C. gracilis)-a marine microalga-is rich in proteins, fucoxanthin, and eicosapentaenoic acid (EPA). Growing evidence indicates that dietary fucoxanthin and EPA have beneficial effects in humans. However, none of these studies have shown that dietary C. gracilis has beneficial effects in mammals. In this study, we investigated the effects of dietary C. gracilis on lipid abnormalities in Sprague-Dawley rats fed a high-sucrose cholesterol-containing diet. Dried C. gracilis was added to the control diet at a final dose of 2 or 5% (w/w). After four weeks, the soleus muscle weights were found to be dose-responsive to C. gracilis and showed a tendency to increase. The hepatic triglyceride and total cholesterol levels were significantly reduced by C. gracilis feeding compared to those in the control group. The activities of FAS and G6PDH, which are related to fatty acid de novo synthesis, were found to be dose-responsive to C. gracilis and tended to decrease. The hepatic glycerol content was also significantly decreased by C. gracilis feeding, and the serum HDL cholesterol levels were significantly increased, whereas the serum levels of cholesterol absorption markers (i.e., campesterol and β-sitosterol) and the hepatic mRNA levels of Scarb1 were significantly decreased. Water-soluble metabolite analysis showed that the muscular contents of several amino acids, including leucine, were significantly increased by C. gracilis feeding. The tendency toward an increase in the weight of the soleus muscle as a result of C. gracilis feeding may be due to the enhancement of muscle protein synthesis centered on leucine. Collectively, these results show that the oral administration of C. gracilis alleviates hepatic lipid accumulation in rats fed a high-sucrose and cholesterol-containing diet, indicating the potential use of C. gracilis as a food resource.

Metabolomics-based response of Salmonella to desiccation stress and skimmed milk powder storage.

The strong survival ability of Salmonella in low-moisture foods (LMFs) has been of public concern, and is considered a threat to people's health. Recently, the development of omics technology has promoted research on the molecular mechanisms of the desiccation stress response of pathogenic bacteria. However, multiple analytical aspects related to their physiological characteristics remain unclear. We explored the physiological metabolism changes of S. enterica Enteritidis exposed to a 24 h-desiccation treatment and a subsequent 3-month desiccation storage in skimmed milk powder (SMP) with an approach of gas chromatography-mass spectrometry (GC-MS) and ultra-performance liquid chromatography-Q Exactive-mass spectrometry (UPLC-QE-MS). A total of 8,292 peaks were extracted, of which 381 were detected by GC-MS and 7,911 peaks were identified by LC-MS/MS, respectively. Through analyses of differentially expressed metabolites (DEMs) and key pathways, a total of 58 DEMs emerged from the 24 h-desiccation treatment, which exhibited the highest relevance for five metabolic pathways, involving glycine, serine, and threonine metabolism, pyrimidine metabolism, purine metabolism, vitamin B6 metabolism, and pentose phosphate pathway. After 3-month SMP storage, 120 DEMs were identified, which were related to several regulatory pathways including arginine and proline metabolism, serine and threonine metabolism, β-alanine metabolism, glycerolipid metabolism, and glycolysis. The analyses of key enzyme activities of XOD, PK, and G6PDH and ATP content provided further evidence that supported the metabolic responses such as nucleic acid degradation, glycolysis, and ATP production played an important role in Salmonella's adaptation to desiccation stress. This study enables a better understanding of metabolomics-based responses of Salmonella at the initial stage of desiccation stress and the following long-term adaptive stage. Meanwhile, the identified discriminative metabolic pathways may serve as potentially useful targets in developing strategies for the control and prevention of desiccation-adapted Salmonella in LMFs.

An Innovative Mei-Gin Formula Exerts Anti-Adipogenic and Anti-Obesity Effects in 3T3-L1 Adipocyte and High-Fat Diet-Induced Obese Rats

To investigate the potential anti-obesity properties of an innovative functional formula (called the Mei-Gin formula: MGF) consisting of bainiku-ekisu, Prunus mume (70% ethanol extract), black garlic (water extract), and Mesona procumbens Hemsl. (40% ethanol extract) for reducing lipid accumulation in 3T3-L1 adipocytes in vitro and obese rats in vivo. The prevention and regression of high-fat diet (HFD)-induced obesity by the intervention of Japan Mei-Gin, MGF-3 and -7, and positive health supplement powder were investigated in male Wistar rats. The anti-obesity effects of MGF-3 and -7 in rats with HFD-induced obesity were examined by analyzing the role of visceral and subcutaneous adipose tissue in the development of obesity. The results indicated that MGF-1-7 significantly suppressed lipid accumulation and cell differentiation through the down-regulation of GPDH activity, as a key regulator in the synthesis of triglycerides. Additionally, MGF-3 and MGF-7 exhibited a greater inhibitory effect on adipogenesis in 3T3-L1 adipocytes. The high-fat diet increased body weight, liver weight, and total body fat (visceral and subcutaneous fat) in obese rats, while these alterations were effectively improved by the administration of MGF-3 and -7, especially MGF-7. This study highlights the role of the Mei-Gin formula, particularly MGF-7, in anti-obesity action, which has the potential to be used as a therapeutic agent for the prevention or treatment of obesity.

Effects of microplastic combined with Cr(III) on apoptosis and energy pathway of coral endosymbiont.

The combined effect of polyethylene (PE) microplastics and chromium (Cr(III)) on the scleractinian coral Acropora pruinosa (A. pruinosa) was investigated. The endpoints analysed in this study included the endosymbiont density, the chlorophyll a + c content, and the activity of enzymes involved in apoptosis (caspase-1, caspase-3), glycolysis (lactate dehydrogenase, LDH), the pentose phosphate pathway (glucose-6-phosphate dehydrogenase, G6PDH) and electron transfer coenzyme (nicotinamide adenine dinucleotide, NAD+/NADH). During the 7-day exposure to PE and Cr(III) stress, the endosymbiont density and chlorophyll content decreased gradually. The caspase-1 and caspase-3 activities increased in the high-concentration Cr(III) exposure group. Furthermore, the LDH and G6PDH activities decreased significantly, and the NAD+/NADH was decreased significantly. In summary, the results showed that PE and Cr(III) stress inhibited the endosymbiont energy metabolism enzymes and further led to endosymbiont apoptosis in coral. In addition, under exposure to the combination of stressors, when the concentration of Cr(III) remained at 1 × 10-2mg/L, the toxic effects of heavy metals on the endosymbiont were temporarily relieved with elevated PE concentrations. In contrast, when coral polyps were exposed to 5mg/L PE and increasing Cr(III) concentrations, their metabolic activities were seriously disturbed, which increased the burden of energy consumption. In the short term, the toxic effect of Cr(III) was more obvious than that of PE because Cr(III) exposure leads to endosymbiont apoptosis and irreversible damage. This is the first study to provide insights into the combined effect of microplastic and Cr(III) stress on the apoptosis and energy pathways of coral endosymbionts. This study suggested that microplastics combined with Cr(III) are an important factor affecting the apoptosis and energy metabolism of endosymbionts, accelerating the collapse of the balance between the coral host and symbiotic endosymbiont.

Elevated atmospheric CO2 concentration changes the eco-physiological response of barley to polystyrene nanoplastics

The impacts of plastic particles are being extensively studied, especially in agro-ecosystem. In the simulating experiment, elevated atmospheric CO2 concentration (e[CO2], 800 μmol mol−1) increased nanoplastics (NPs, red fluorescently labeled polystyrene, 95 nm) concentration in NPs-treated roots from 0.0082 mg g−1 to 0.0275 mg g−1. The H2O2 concentrations in NPs-treated leaves and roots were decreased by 28.41 % and 43.29 % responding to e[CO2], due to the intervention of antioxidant enzymes. In NPs-treated plants, e[CO2] increased Pn, Ci and carotenoid concentration by 10.97 %, 118.07 % and 40.83 %, while decreased gs and Tr by 36.36 % and 32.55 %. e[CO2] weakened NPs-induced modulation of photosynthetic light reaction via causing less electron production, but induced higher Ci promoting the Calvin-Benson cycle in NPs-treated plants. In the presence of NPs exposure, e[CO2] aggravated the reduction in glycolysis by decreasing the activities of cytInv, vacInv, cwInv, AGPase, UGPase, PGM, PGI, G6PDH, PFK and Ald, while suppressed the efficiency of tricarboxylic acid and biological oxidation due to the decreased activities of CS, ICDH, α-KGDH, NADH dehydrogenase, succinate dehydrogenase, cytochrome c oxidase and ATP synthase. The results showed the landscapes by which e[CO2] sculpt the eco-physiological response of barley plant to NPs, and provided key insights into the agricultural sustainability in the future under emerging pollution and environmental changes.

Characterization of controlled-release Eucalyptus citriodora oil/Zinc ions nanoparticles with enhanced antibacterial properties against E. coli O157:H7 in fruit juice

Eucalyptus citriodora oil (ECO) has excellent antibacterial properties, but its application is limited due to its volatility and lack of antimicrobial targeting properties. Zinc ions are metal ions on which the active center of metalloproteinases depend and have antibacterial functions. This study aimed to prepare nanoparticles against Escherichia coli O157:H7 (E. coli O157:H7) by encapsulating ECO in zein with nano-precipitation method, and chelating zinc metal ions with electrostatic interaction to improve the stability, controlled-release ability and antibacterial ability of nanoparticles. Herein, the antibacterial mechanism of ECO against E. coli O157:H7 was investigated from the molecular level. The results of molecular docking showed that ECO inhibited the activity of G6PDH in respiratory metabolism pathway (hexose monophophate pathway), and also inhibited the DNA polymerase. Furthermore, we demonstrated that the controlled-release nanoparticles (ECO/Zn2+-loaded NPT) possessed suitable particle size (275.43 nm), poly dispersity index (PDI, 0.254), zeta potential (-31.12 mV) and chelation rate (42.3 %). The results of Fourier Transform Infrared spectrometer (FT-IR), and Raman spectrum confirmed that ECO was successfully encapsulated in the nanoparticles. Meanwhile, the results of antibacterial experiments showed that ECO/Zn2+-loaded NPT possessed better antibacterial activity than ECO/zein nanoparticles. Finally, the test of application in fruit juice indicated that ECO/Zn2+-loaded NPT had no significant effect on physico-chemical properties and exhibited potential application in juice preservation.