scholarly journals Dynamics of Energy Metabolism in Carbon Starvation-Induced Fruitlet Abscission in Litchi

Horticulturae ◽  
2021 ◽  
Vol 7 (12) ◽  
pp. 576
Author(s):  
Qian Wu ◽  
Xingshuai Ma ◽  
Qingxin Chen ◽  
Ye Yuan ◽  
Huicong Wang ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Citrate Synthase ◽  
Tca Cycle ◽  
Carbon Starvation ◽  
Fruit Abscission ◽  
Oxidative Phosphorylation Pathway ◽  
Glycolysis Pathway ◽  
Liquid Chromatography Tandem Mass ◽  
Fruitlet Abscission

Fruit abscission is triggered by multiple changes in endogenous components of the fruit, including energy metabolism. However, it is still unknown how the core energy metabolism pathways are modified during fruit abscission. Here, we investigated the relationship between carbon starvation-induced fruitlet abscission and energy metabolism changes in litchi. The fruitlet abscission of litchi ‘Feizixiao’ was induced sharply by girdling plus defoliation (GPD), a carbon stress treatment. Using liquid chromatography tandem mass spectrometry (LC-MS/MS) targeted metabolomics analysis, we identified a total of 21 metabolites involved in glycolysis, TCA cycle and oxidative phosphorylation pathways. Among them, the content of most metabolites in glycolysis pathways and TCA cycles was reduced, and the activity of corresponding metabolic enzymes such as ATP-dependent phosphofructokinase (ATP-PFK), pyruvate kinase (PK), citrate synthase (CS), succinate thiokinase (SAT), and NAD-dependent malate dehydrogenase (NAD-MDH) was decreased. Consistently, we further showed that the expression of the relative genes (LcPFK2, LcPK2, LcPK4, LcCS1, LcCS2, LcSAT, LcMDH1 and LcMDH2) was also significantly down-regulated. In contrast, the level of ATP, an important metabolite in the oxidative phosphorylation pathway, was elevated in parallel with both higher activity of H+-ATPase and the increased expression level of LcH+-ATPase1. In conclusion, our findings suggest that carbon starvation can induce fruitlet abscission in litchi probably by energy depletion that mediated through both the suppression of the glycolysis pathway and TCA cycle and the enhancement of the oxidative phosphorylation pathway.

scholarly journals Energy Metabolism in the Bone is Associated with Histomorphometric Changes in Rats with Hyperthyroidism

2018 ◽  
Vol 46 (4) ◽  
pp. 1471-1482 ◽  
Author(s):  
Zhuoqing Hu ◽  
Minqun Du ◽  
Wenxiu Lai ◽  
Yanlong Liang ◽  
Qin Liu ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Tca Cycle ◽  
Biomechanical Properties ◽  
Male Rats ◽  
Mineral Apposition Rate ◽  
Tartrate Resistant Acid Phosphatase ◽  
Mineral Density ◽  
Bone Formation Rate ◽  
Volume Percentage

Background/Aims: In this study we assessed histomorphometric changes induced by thyroxine (T4) in 3-month-old hyperthyroid male rats and examined whether the potential mechanism of these changes is related to bone changes. Methods: Rats were classified as either hyperthyroid following administration of 250 µg/kg/day freshly prepared T4 by gavage for 2 months or euthyroid following administration of vehicle alone (n = 8 per group). We measured bone mineral density (BMD), bone biomechanical properties, and bone histomorphometric changes. Levels of serum indicators were also measured, and three right femurs from the two groups were selected for proteomic investigation. Results: Compared with the control rats, hyperthyroid rats showed a reduction in the fifth lumbar vertebral BMD as well as in the entire femoral BMD (p = 0.033 and 0.026, respectively). Histomorphometric analysis of the proximal tibial metaphysis showed that the percentage of the trabecular area, trabecular number, and percentage of the cortical bone area in the hyperthyroid rats significantly decreased compared with those of the control rats. Conversely, bone formation rate (per unit of bone surface and bone volume), percentage of the osteoclast perimeter, trabecular separation, and endosteal mineral apposition rate in the hyperthyroid rats significantly increased compared with the control rats (all p < 0.05). Except for stiffness (p = 0.24), all bone biomechanical properties of the femur showed a significant decreasing trend in the hyperthyroid rats versus the control rats (all p < 0.05). Serum levels of osteocalcin, alkaline phosphatase, terminal telopeptides of type β collagen, and tartrate-resistant acid phosphatase were higher in the hyperthyroid rats than in the control rats (all p < 0.05). Using isobaric tags for relative and absolute quantification (iTRAQ), the expression levels of 1,310 proteins were found to be significantly different between the hyperthyroid and control rats (711 proteins were upregulated and 599 were downregulated in hyperthyroid rats). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses showed that most of the enzymes in the glycolysis–tricarboxylic acid (TCA) cycle–oxidative phosphorylation signalling pathway were upregulated in hyperthyroid rats, and seven differentially expressed proteins were selected to verify the iTRAQ results using western blotting. Conclusion: Energy metabolism via the glycolysis–TCA cycle–oxidative phosphorylation pathway is positively associated with T4-induced bone histomorphometric changes in rats.

scholarly journals Targeting Energy Metabolism in Mycobacterium tuberculosis, a New Paradigm in Antimycobacterial Drug Discovery

mBio ◽  
2017 ◽  
Vol 8 (2) ◽  
Author(s):  
Dirk Bald ◽  
Cristina Villellas ◽  
Ping Lu ◽  
Anil Koul
Keyword(s):  
Drug Discovery ◽  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Multidrug Resistant ◽  
New Paradigm ◽  
Mycobacterial Infections ◽  
Highly Active ◽  
Oxidative Phosphorylation Pathway ◽  
Novel Target ◽  
Synthase Inhibitor

ABSTRACT Drug-resistant mycobacterial infections are a serious global health challenge, leading to high mortality and socioeconomic burdens in developing countries worldwide. New innovative approaches, from identification of new targets to discovery of novel chemical scaffolds, are urgently needed. Recently, energy metabolism in mycobacteria, in particular the oxidative phosphorylation pathway, has emerged as an object of intense microbiological investigation and as a novel target pathway in drug discovery. New classes of antibacterials interfering with elements of the oxidative phosphorylation pathway are highly active in combating dormant or latent mycobacterial infections, with a promise of shortening tuberculosis chemotherapy. The regulatory approval of the ATP synthase inhibitor bedaquiline and the discovery of Q203, a candidate drug targeting the cytochrome bc 1 complex, have highlighted the central importance of this new target pathway. In this review, we discuss key features and potential applications of inhibiting energy metabolism in our quest for discovering potent novel and sterilizing drug combinations for combating tuberculosis. We believe that the combination of drugs targeting elements of the oxidative phosphorylation pathway can lead to a completely new regimen for drug-susceptible and multidrug-resistant tuberculosis.

scholarly journals Inhibition of glycerol metabolism in hepatocytes isolated from endotoxic rats

1997 ◽  
Vol 325 (2) ◽  
pp. 519-525 ◽  
Author(s):  
Pascale LECLERCQ ◽  
Céline FILIPPI ◽  
Brigitte SIBILLE ◽  
Sarah HAMANT ◽  
Christiane KERIEL ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Kinase Activity ◽  
Glycerol Metabolism ◽  
Transcription Rate ◽  
Intact Cells ◽  
Cellular Volume ◽  
Main Effect ◽  
Oxidative Phosphorylation Pathway

Sepsis or endotoxaemia inhibits gluconeogenesis from various substrates, the main effect being related to a change in the phosphoenolpyruvate carboxykinase transcription rate. In addition, sepsis has been reported to affect the oxidative phosphorylation pathway. We have studied glycerol metabolism in hepatocytes isolated from rats fasted and injected 16 h previously with lipopolysaccharide from Escherichiacoli. Endotoxin inhibited glycerol metabolism and led to a very large accumulation of glycerol 3-phosphate; the cytosolic reducing state was increased. Furthermore glycerol kinase activity was increased by 33% (P < 0.01). The respiratory rate of intact cells was significantly decreased by sepsis, with glycerol or octanoate as exogenous substrates, whereas oxidative phosphorylation (ATP-to-O ratio or respirations in state 4, state 3 and the oligomycin-insensitive state as well as the uncoupled state) was unchanged in permeabilized hepatocytes. Hence the effect on energy metabolism seems to be present only in intact hepatocytes. An additional important feature was the observation of a significant increase in cellular volume in cells from endotoxic animals, which might account for the alterations induced by sepsis.

scholarly journals The Effects of Storage in vitro on Functions, Transcriptome, Proteome, and Oxidation Resistance of Giant Grouper Sperm

2021 ◽  
Vol 8 ◽  
Author(s):  
Yang Yang ◽  
Tong Wang ◽  
Sen Yang ◽  
Xi Wu ◽  
Wenhua Huang ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Oxidation Resistance ◽  
Cold Storage ◽  
Prolonged Storage ◽  
Negative Effects ◽  
Normal Functions ◽  
Oxidative Phosphorylation Pathway ◽  
The Absolute

Asynchrony of sexual maturity is a huge limitation in the reproduction of grouper sperm. Cold storage of sperm is an effective method to solve the problem of asynchronization. However, sperms gradually lose their activity with the prolonged storage time in vitro. In order to explore causes, the effects of cold storage on transcriptome, proteome and oxidation resistance of giant grouper sperm were analyzed. Firstly, the absolute RNA quantity and consistent transcripts existed in each spermatozoon were estimated. With the prolonged storage, the RNA quantity gradually decreased both in the cytoplasm and in the mitochondria of the spermatozoon. The decreased transcripts were mainly enriched with energy metabolism and stress response. Similar to RNAs, the absolute protein quantity was also significantly decreased during the storage of sperm. Decreased proteins were mainly enriched with the oxidative phosphorylation pathway. Proteins involved in the oxidative phosphorylation showed a faster degradation rate compared to the average total protein. In addition, the oxidation resistance and adenosine triphosphate (ATP) contents showed a significant decrease in the sperm during storage in vitro. These results implied that damages of transcriptome, proteome, and oxidation resistance have negative effects on the normal functions of sperm, especially their energy metabolism. The present study provides essential foundation for improving the storage of sperm in vitro.

The STAT3-MYC Axis Promotes Survival of Leukemia Stem Cells by Regulating SLC1A5 and Oxidative Phosphorylation

Blood ◽  
2021 ◽  
Author(s):  
Maria Amaya ◽  
Anagha Inguva ◽  
Shanshan Pei ◽  
Courtney L Jones ◽  
Anna Krug ◽  
...  
Keyword(s):  
Stem Cells ◽  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Tca Cycle ◽  
Leukemia Stem Cells ◽  
Specific Expression ◽  
Neutral Amino Acid Transporter ◽  
Stem And Progenitor Cells ◽  
Stat3 Inhibition

AML is characterized by the presence of leukemia stem cells (LSCs), and failure to fully eradicate this population contributes to disease persistence/relapse. Prior studies have characterized metabolic vulnerabilities of LSCs, which demonstrate preferential reliance on oxidative phosphorylation (OXPHOS) for energy metabolism and survival. In the present study, using both genetic and pharmacologic strategies in primary human AML specimens, we show that signal transducer and activator of transcription 3 (STAT3) mediates OXPHOS in LSCs. STAT3 regulates AML-specific expression of MYC, which in turn controls transcription of the neutral amino acid transporter SLC1A5. We show that genetic inhibition of MYC or SLC1A5 acts to phenocopy the impairment of OXPHOS observed with STAT3 inhibition, thereby establishing this axis as a regulatory mechanism linking STAT3 to energy metabolism. Inhibition of SLC1A5 reduces intracellular levels of glutamine, glutathione and multiple TCA metabolites, leading to reduced TCA cycle activity and inhibition of OXPHOS. Based on these findings, we used a novel small molecule STAT3 inhibitor, that binds STAT3 and disrupts STAT3-DNA, to evaluate the biological role of STAT3. We show that STAT3 inhibition selectively leads to cell death in AML stem and progenitor cells derived from newly diagnosed and relapsed patients, while sparing normal hematopoietic cells. Together, these findings establish a STAT3-mediated mechanism that controls energy metabolism and survival in primitive AML cells.

Role of Quercetin in Mitigation of Lindane Induced Toxicity in Terms of Oxidative Responses and Metabolic Status in Mice Brain

2020 ◽  
Vol 16 ◽  
Author(s):  
Anupama Sharma ◽  
Renu Bist ◽  
Hemant Pareek
Keyword(s):  
Citrate Synthase ◽  
Thiobarbituric Acid ◽  
Tca Cycle ◽  
Treated Group ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Mice Brain ◽  
The Brain ◽  
Oxidative Responses

Background:: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective:: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods:: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results:: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion:: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.

Schisandrin Restores the Amyloid β-Induced Impairments on Mitochondrial Function, Energy Metabolism, Biogenesis, and Dynamics in Rat Primary Hippocampal Neurons

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhongyuan Piao ◽  
Lin Song ◽  
Lifen Yao ◽  
Limei Zhang ◽  
Yichan Lu
Keyword(s):  
Energy Metabolism ◽  
Cytochrome C ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Citrate Synthase ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Mitochondrial Functions ◽  
Primary Hippocampal Neurons

Introduction: Schisandrin which is derived from Schisandra chinensis has shown multiple pharmacological effects on various diseases including Alzheimer’s disease (AD). It is demonstrated that mitochondrial dysfunction plays an essential role in the pathogenesis of neurodegenerative disorders. Objective: Our study aims to investigate the effects of schisandrin on mitochondrial functions and metabolisms in primary hippocampal neurons. Methods: In our study, rat primary hippocampal neurons were isolated and treated with indicated dose of amyloid β1–42 (Aβ1–42) oligomer to establish a cell model of AD in vitro. Schisandrin (2 μg/mL) was further subjected to test its effects on mitochondrial function, energy metabolism, mitochondrial biogenesis, and dynamics in the Aβ1–42 oligomer-treated neurons. Results and Conclusions: Our findings indicated that schisandrin significantly alleviated the Aβ1–42 oligomer-induced loss of mitochondrial membrane potential and impaired cytochrome c oxidase activity. Additionally, the opening of mitochondrial permeability transition pore and release of cytochrome c were highly restricted with schisandrin treatment. Alterations in cell viability, ATP production, citrate synthase activity, and the expressions of glycolysis-related enzymes demonstrated the relief of defective energy metabolism in Aβ-treated neurons after the treatment of schisandrin. For mitochondrial biogenesis, elevated expression of peroxisome proliferator-activated receptor γ coactivator along with promoted mitochondrial mass was found in schisandrin-treated cells. The imbalance in the cycle of fusion and fission was also remarkably restored by schisandrin. In summary, this study provides novel mechanisms for the protective effect of schisandrin on mitochondria-related functions.

scholarly journals Butyrate Prevents TGF-β1-Induced Alveolar Myofibroblast Differentiation and Modulates Energy Metabolism

Metabolites ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 258
Author(s):  
Hyo Yeong Lee ◽  
Somi Nam ◽  
Mi Jeong Kim ◽  
Su Jung Kim ◽  
Sung Hoon Back ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Pulmonary Fibrosis ◽  
Transforming Growth Factor ◽  
Mitochondrial Dynamics ◽  
Tca Cycle ◽  
Lung Fibroblasts ◽  
Myofibroblast Differentiation ◽  
Pulmonary Fibroblasts ◽  
Matrix Deposition ◽  
Tgf Β1

Idiopathic pulmonary fibrosis (IPF) is a serious lung disease characterized by excessive collagen matrix deposition and extracellular remodeling. Signaling pathways mediated by fibrotic cytokine transforming growth factor β1 (TGF-β1) make important contributions to pulmonary fibrosis, but it remains unclear how TGF-β1 alters metabolism and modulates the activation and differentiation of pulmonary fibroblasts. We found that TGF-β1 lowers NADH and NADH/NAD levels, possibly due to changes in the TCA cycle, resulting in reductions in the ATP level and oxidative phosphorylation in pulmonary fibroblasts. In addition, we showed that butyrate (C4), a short chain fatty acid (SCFA), exhibits potent antifibrotic activity by inhibiting expression of fibrosis markers. Butyrate treatment inhibited mitochondrial elongation in TGF-β1-treated lung fibroblasts and increased the mitochondrial membrane potential (MMP). Consistent with the mitochondrial observations, butyrate significantly increased ADP, ATP, NADH, and NADH/NAD levels in TGF-β1-treated pulmonary fibroblasts. Collectively, our findings indicate that TGF-β1 induces changes in mitochondrial dynamics and energy metabolism during myofibroblast differentiation, and that these changes can be modulated by butyrate, which enhances mitochondrial function.

scholarly journals Metabolomic Analysis to Elucidate Mechanisms of Sunitinib Resistance in Renal Cell Carcinoma

Metabolites ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 1
Author(s):  
Tomonori Sato ◽  
Yoshihide Kawasaki ◽  
Masamitsu Maekawa ◽  
Shinya Takasaki ◽  
Kento Morozumi ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Energy Metabolism ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Progression ◽  
Renal Cell ◽  
Treatment Resistance ◽  
Tca Cycle ◽  
Glutamine Uptake

Metabolomics analysis possibly identifies new therapeutic targets in treatment resistance by measuring changes in metabolites accompanying cancer progression. We previously conducted a global metabolomics (G-Met) study of renal cell carcinoma (RCC) and identified metabolites that may be involved in sunitinib resistance in RCC. Here, we aimed to elucidate possible mechanisms of sunitinib resistance in RCC through intracellular metabolites. We established sunitinib-resistant and control RCC cell lines from tumor tissues of RCC cell (786-O)-injected mice. We also quantified characteristic metabolites identified in our G-Met study to compare intracellular metabolism between the two cell lines using liquid chromatography-mass spectrometry. The established sunitinib-resistant RCC cell line demonstrated significantly desuppressed protein kinase B (Akt) and mesenchymal-to-epithelial transition (MET) phosphorylation compared with the control RCC cell line under sunitinib exposure. Among identified metabolites, glutamine, glutamic acid, and α-KG (involved in glutamine uptake into the tricarboxylic acid (TCA) cycle for energy metabolism); fructose 6-phosphate, D-sedoheptulose 7-phosphate, and glucose 1-phosphate (involved in increased glycolysis and its intermediate metabolites); and glutathione and myoinositol (antioxidant effects) were significantly increased in the sunitinib-resistant RCC cell line. Particularly, glutamine transporter (SLC1A5) expression was significantly increased in sunitinib-resistant RCC cells compared with control cells. In this study, we demonstrated energy metabolism with glutamine uptake and glycolysis upregulation, as well as antioxidant activity, was also associated with sunitinib resistance in RCC cells.

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