Interrelationship between the pentose phosphate pathway and nucleotide synthesis in cultured cells of Catharanthus roseus

1984 ◽  
Vol 35 (2) ◽  
pp. 123-126 ◽  
Author(s):  
Fumiko Hirose ◽  
Hiroshi Ashihara
Keyword(s):  
Catharanthus Roseus ◽  
Pentose Phosphate Pathway ◽  
Cultured Cells ◽  
Pentose Phosphate ◽  
Nucleotide Synthesis

scholarly journals Annurca Apple Polyphenols Ignite Keratin Production in Hair Follicles by Inhibiting the Pentose Phosphate Pathway and Amino Acid Oxidation

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1406 ◽  
Author(s):  
Nadia Badolati ◽  
Eduardo Sommella ◽  
Gennaro Riccio ◽  
Emanuela Salviati ◽  
Dimitri Heintz ◽  
...  
Keyword(s):  
Pentose Phosphate Pathway ◽  
Hair Growth ◽  
High Resolution Mass Spectrometry ◽  
Negative Impact ◽  
Adult Population ◽  
Pentose Phosphate ◽  
Hair Follicles ◽  
Acid Oxidation ◽  
Healthy Human ◽  
Nucleotide Synthesis

Patterned hair loss (PHL) affects around 50% of the adult population worldwide. The negative impact that this condition exerts on people’s life quality has boosted the appearance of over-the-counter products endowed with hair-promoting activity. Nutraceuticals enriched in polyphenols have been recently shown to promote hair growth and counteract PHL. Malus pumila Miller cv. Annurca is an apple native to Southern Italy presenting one of the highest contents of Procyanidin B2. We have recently shown that oral consumption of Annurca polyphenolic extracts (AAE) stimulates hair growth, hair number, hair weight and keratin content in healthy human subjects. Despite its activity, the analysis of the molecular mechanism behind its hair promoting effect is still partially unclear. In this work we performed an unprecedented metabolite analysis of hair follicles (HFs) in mice topically treated with AAE. The metabolomic profile, based on a high-resolution mass spectrometry approach, revealed that AAE re-programs murine HF metabolism. AAE acts by inhibiting several NADPH dependent reactions. Glutaminolysis, pentose phosphate pathway, glutathione, citrulline and nucleotide synthesis are all halted in vivo by the treatment of HFs with AAE. On the contrary, mitochondrial respiration, β-oxidation and keratin production are stimulated by the treatment with AAE. The metabolic shift induced by AAE spares amino acids from being oxidized, ultimately keeping them available for keratin biosynthesis.

scholarly journals Role of Intracellular Carbon Metabolism Pathways in Shigella flexneri Virulence

2014 ◽  
Vol 82 (7) ◽  
pp. 2746-2755 ◽  
Author(s):  
E. A. Waligora ◽  
C. R. Fisher ◽  
N. J. Hanovice ◽  
A. Rodou ◽  
E. E. Wyckoff ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Pentose Phosphate Pathway ◽  
Carbon Metabolism ◽  
Cultured Cells ◽  
Shigella Flexneri ◽  
Plaque Assay ◽  
Pentose Phosphate ◽  
Host Cells ◽  
Content Type ◽  
Pathway Gene

ABSTRACTShigella flexneri, which replicates in the cytoplasm of intestinal epithelial cells, can use the Embden-Meyerhof-Parnas, Entner-Doudoroff, or pentose phosphate pathway for glycolytic carbon metabolism. To determine which of these pathways is used by intracellularS. flexneri, mutants were constructed and tested in a plaque assay for the ability to invade, replicate intracellularly, and spread to adjacent epithelial cells. Mutants blocked in the Embden-Meyerhof-Parnas pathway (pfkABandpykAFmutants) invaded the cells but formed very small plaques. Loss of the Entner-Doudoroff pathway geneedaresulted in small plaques, but the doubleeda eddmutant formed normal-size plaques. This suggested that the plaque defect of theedamutant was due to buildup of the toxic intermediate 2-keto-3-deoxy-6-phosphogluconic acid rather than a specific requirement for this pathway. Loss of the pentose phosphate pathway had no effect on plaque formation, indicating that it is not critical for intracellularS. flexneri. Supplementation of the epithelial cell culture medium with pyruvate allowed the glycolysis mutants to form larger plaques than those observed with unsupplemented medium, consistent with data from phenotypic microarrays (Biolog) indicating that pyruvate metabolism was not disrupted in these mutants. Interestingly, the wild-typeS. flexnerialso formed larger plaques in the presence of supplemental pyruvate or glucose, with pyruvate yielding the largest plaques. Analysis of the metabolites in the cultured cells showed increased intracellular levels of the added compound. Pyruvate increased the growth rate ofS. flexneriin vitro, suggesting that it may be a preferred carbon source inside host cells.

Pentose phosphate pathway in cellular trophoblasts from full-term human placentas

1991 ◽  
Vol 261 (6) ◽  
pp. C1042-C1047 ◽  
Author(s):  
A. J. Moe ◽  
D. R. Farmer ◽  
D. M. Nelson ◽  
C. H. Smith
Keyword(s):  
Amino Acids ◽  
Methylene Blue ◽  
Glucose Metabolism ◽  
Electron Acceptor ◽  
Pentose Phosphate Pathway ◽  
Cultured Cells ◽  
Minor Component ◽  
Pentose Phosphate ◽  
Full Term ◽  
A Minor

Glucose metabolism was investigated in cellular trophoblasts isolated from full-term human placentas. The specific yields of 14CO2 from D-[1-14C]glucose and D-[6-14C]glucose were used to determine glucose metabolism via the pentose cycle for cells freshly isolated or cells grown in culture for 1 and 3 days. Cells were mononucleated on day 1 but fused to form multinucleated syncytiotrophoblasts by day 3. The principal product of glucose metabolism under all conditions was lactate, accounting for approximately three-fourths of recovered 14C in products. Pentose cycle activity contributed 0.57 +/- 0.01, 0.39 +/- 0.06, and 0.21 +/- 0.05% of the glucose metabolized by cells freshly isolated, cultured for 1 day, and cultured for 3 days, respectively. In the presence of the electron acceptor methylene blue, pentose cycle activity increased to 16.5 +/- 2.1, 13.8 +/- 1.5, and 18.2 +/- 1.7% for cells freshly isolated, cultured for 1 day, and cultured for 3 days, respectively. Trace amounts of 14C were recovered in other products including amino acids and glycogen. These data suggest that pentose cycle activity in cellular trophoblasts from full-term placenta, like those in full-term villous tissue, is a minor component of glucose metabolism. However, these cultured cells maintain a capacity to oxidize glucose via the pentose cycle at relatively high rates.

scholarly journals p53 coordinates DNA repair with nucleotide synthesis by suppressing PFKFB3 expression and promoting the pentose phosphate pathway

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Derek A. Franklin ◽  
Yizhou He ◽  
Patrick L. Leslie ◽  
Andrey P. Tikunov ◽  
Nick Fenger ◽  
...  
Keyword(s):  
Dna Repair ◽  
Pentose Phosphate Pathway ◽  
Pentose Phosphate ◽  
Nucleotide Synthesis

scholarly journals The Pentose Phosphate Pathway in Cancer: Regulation and Therapeutic Opportunities

Chemotherapy ◽  
2021 ◽  
pp. 1-13
Author(s):  
Noorhan Ghanem ◽  
Chirine El-Baba ◽  
Khaled Araji ◽  
Riyad El-Khoury ◽  
Julnar Usta ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Pentose Phosphate Pathway ◽  
Aerobic Glycolysis ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Pentose Phosphate ◽  
Nucleotide Synthesis ◽  
Intermediary Metabolites ◽  
Dividing Cells ◽  
Metabolites Production ◽  
Reductive Metabolism

<b><i>Background:</i></b> Tumorigenesis is associated with deregulation of nutritional requirements, intermediary metabolites production, and microenvironment interactions. Unlike their normal cell counterparts, tumor cells rely on aerobic glycolysis, through the Warburg effect. <b><i>Summary:</i></b> The pentose phosphate pathway (PPP) is a major glucose metabolic shunt that is upregulated in cancer cells. The PPP comprises an oxidative and a nonoxidative phase and is essential for nucleotide synthesis of rapidly dividing cells. The PPP also generates nicotinamide adenine dinucleotide phosphate, which is required for reductive metabolism and to counteract oxidative stress in tumor cells. This article reviews the regulation of the PPP and discusses inhibitors that target its main pathways. <b><i>Key Message:</i></b> Exploiting the metabolic vulnerability of the PPP offers potential novel therapeutic opportunities and improves patients’ response to cancer therapy.

scholarly journals The short isoform of PRLR suppresses the pentose phosphate pathway and nucleotide synthesis through the NEK9-Hippo axis in pancreatic cancer

Theranostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 3898-3915
Author(s):  
Huizhen Nie ◽  
Pei-Qi Huang ◽  
Shu-Heng Jiang ◽  
Qin Yang ◽  
Li-Peng Hu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Pentose Phosphate Pathway ◽  
Pentose Phosphate ◽  
Nucleotide Synthesis

scholarly journals Measurement of pentose phosphate-pathway activity in a single incubation with [1,6-13C2,6,6-2H2]glucose

1994 ◽  
Vol 302 (1) ◽  
pp. 31-38 ◽  
Author(s):  
B D Ross ◽  
P B Kingsley ◽  
O Ben-Yoseph
Keyword(s):  
Pentose Phosphate Pathway ◽  
Cultured Cells ◽  
Krebs Cycle ◽  
Pentose Phosphate ◽  
Repeated Measurements ◽  
Co2 Production ◽  
Spectrometric Analysis ◽  
14Co2 Production ◽  
Single Set

The isotopically substituted molecule D-[1,6-13C2,6,6-2H2]glucose is introduced for measuring the relative activities of the pentose phosphate pathway (PPP) and glycolysis in a single incubation. PPP activity in cultured cells was determined by gas chromatography/mass spectrometric analysis of lactate produced by cells incubated with [1,6-13C2,6,6-2H2]glucose. Two other isotopes, [1,5,6-13C3]glucose and [6-13C,1,6,6-2H3]glucose, were not satisfactory for measurements of this activity. This method has four advantages over the traditional one in which 14CO2 production from [1-14C]glucose and [6-14C]glucose is compared: (1) repeated measurements can be made on a single set of cells, (2) only a single incubation is required, (3) extensive CO2 production by Krebs-cycle activity does not interfere with the measurements and (4) it is not necessary to measure the amount of glucose consumed in order to calculate relative activities of the PPP and glycolysis. Preliminary observation indicates that rat brain PPP activity may be measured in vivo with [1,6-13C2,6,6-2H2]glucose when combined with microdialysis techniques.

scholarly journals Silencing Sirtuin5 induces DNA damage by suppressing the pentose phosphate pathway in a demalonylation-dependent manner: A possible target for anticancer therapy in CRC

2021 ◽  
Author(s):  
Hao-Lian Wang ◽  
Yan Chen ◽  
Yun-Qian Wang ◽  
En-Wei Tao ◽  
Juan Tan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Pentose Phosphate Pathway ◽  
Pentose Phosphate ◽  
Dependent Manner ◽  
Class Iii ◽  
Nucleotide Synthesis ◽  
Cycle Arrest

Abstract A previous study by our research group showed that sirtuin5 (SIRT5), a member of the class III NAD＋-dependent deacetylase family, is highly expressed in colorectal cancer (CRC). The present study showed that deletion of SIRT5 induced cell cycle arrest and apoptosis as a result of continuous and irreparable DNA damage in CRC cells, a consequence of the impaired production of ribose-5-phosphate (R5P) which is essential for nucleotide synthesis. Consistently, the cell cycle arrest and apoptosis induced by SIRT5 silencing could be reversed by supplementation with four nucleotides. Moreover, metabolic profiling revealed that silencing of SIRT5 could inhibit the non-oxidative pentose phosphate pathway (PPP), which produces R5P, required for base ribosylation. Notably, SIRT5 activates transketolase (TKT), the key enzyme in the cellular non-oxidative PPP, by mediating its lysine demalonylation through the interaction between SIRT5 and TKT. Furthermore, the results demonstrated that TKT is essential for the SIRT5-induced malignant phenotypes of CRC, both in vivo and in vitro. These results therefore revealed that the increased lysine malonylation levels of TKT caused by silencing SIRT5 suppresses non-oxidative pentose phosphate metabolism, leading to a low-nucleotide pool. This in turn induces DNA damage in tumor cells and inhibits proliferation, suggesting that SIRT5 may serve as a potential anticancer target.

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