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PubMed1979

Glycolytic activity in human synovial lining cells in rheumatoid arthritis.

It was conceivable that the previously reported elevated pentose-shunt activity in human rheumatoid synoviocytes could be at the expense of glycolytic activity. To test this possibility the activities of glyceraldehyde 3-phosphate and lactate dehydrogenase, the two dehydrogenase enzymes of the latter pathway, have been investigated in the synovial lining cells in fresh sections of nonrheumatoid and rheumatoid synovial tissue. To measure the activity solely in the lining cells, apart from that in underlying infiltrating cells, quantitative cytochemical reactions have been used; the activities were measured by microdensitometry. The results showed highly and significantly increased activity of both enzymes in the rheumatoid cells. Increased activity was also found in synoviocytes in nonrheumatoid synovial tissue after trauma, so that the increased activity of these enzymes is not characteristic of the rheumatoid condition. However, the results indicate that the increased pentose shunt activity in rheumatoid synovial lining cells is not at the expense of glycolytic activity but may be part of an enhanced potential for utilising glucose 6-phosphate in these cells.

Adolescent↗

PubMed1978

Inducing effect of plant cells on nitrogenase activity by Spirillum and Rhizobium in vitro.

Eleven different plant cell tissue cultures of both legume and non-legume origin have been grown in direct association, and in separate but close proximal association with both Spirillum lipoferum and Rhizobium sp. 32H1. Basic similarities were found in the nutritional requirement for the induction of nitrogenase activity (C2H2) in both organisms. In the absence of plant cell cultures both organisms need to be provided with a pentose sugar and a tricarboxylic acid to induce high levels of nitrogen-fixing activity. Plant cell callus tissue appears only capable of supplying the tricarboxylic acid to induce high levels of nitrogen-fixing activity. Plant cell callus tissue appears only capable of supplying the tricarboxylic acids needed but not the sugar component. The plant tissue, however, seems able to activate certain carbohydrates, which in themselves are incapable of substituting for the pentose additive.

Enzyme Induction↗

PubMed1980

Purine synthesis de novo and its regulation in rat hepatocytes.

Purine synthesis de novo and its regulation were studied in freshly isolated hepatocytes from fed adult male rats. The cells incorporated [14C]formate mainly into purine ribonucleotides. The immediate effect of increasing the concentration of inorganic phosphate in the incubation medium was an increase in 5-phosphoribosyl 1-pyrophosphate (PP-ribose-P) availability and a stimulation of purine synthesis de novo. However, prolonged incubation of cells in 25 mM phosphate resulted in a decreased PP-ribose-P availability and purine synthesis de novo. Methylene blue and phenazine methosulfate decreased PP-ribose-P availability and purine synthesis de novo although they stimulated considerably the pentose phosphate pathway. In contrast, epinephrine and glucagon increased significantly PP-ribose-P availability and purine synthesis de novo, but they did not change the activity of the pentose phosphate pathway. These results show a relationship between PP-ribose-P availability and purine synthesis de novo in rat hepatocytes. They emphasize the complexity of the regulation of PP-ribose-P availability.

Animals↗

PubMed1998

Purification and kinetic characterization of hexokinase and glucose-6-phosphate dehydrogenase from Schizosaccharomyces pombe.

Hexokinase and D-glucose-6-phosphate dehydrogenase (G6PDH) from Schizosaccharomyces pmbe have been purified 250-fold by an identical three-step. Both enzymes are dimeric with a molecular mass of 88 kDa for the kinase and 112 kDa for the dehydrogenase. Steady-state kinetic studies were performed on hexokinase and G6PDH, which form the glucose phosphate branch of the oxidative pentose phosphate pathway of S. pombe (fission yeast). Hexokinase promotes Mg(2+)-activated phosphorylation of D-glucose by the equilibrium random Bi Bi mechanism with formation of the abortive enzyme-ADP-glucose complex. ADP inhibits the kinase competitively versus ATP and noncompetitively versus D-glucose. The Mg2+ activation of hexokinase is associated with an increase in the maximal velocity by its interaction with the ternary complex to facilitate the transfer of the phosphoryl group. G6PDH catalyzes NADP(+)-linked oxidation of D-glucose-6-phosphate by the ordered Bi Bi mechanism with NADP+ as the leading reactant. High NADP+ concentration inhibits the dehydrogenase by forming the dead-end ternary complex. In addition, G6PDH is also subjected to product inhibition by NADPH and noncompetitive inhibition by A(G)TP. Thus, the oxidative pentose phosphate pathway in S. pombe may be regulated via inhibition of hexokinase by ADP in conjunction with inhibition of G6PDH by NADPH and ATP.

Glucosephosphate Dehydrogenase↗

PubMed1998

Regulation of D-glucose-6-phosphate dehydrogenase from Schizosaccharomyces pombe.

D-Glucose-6-phosphate dehydrogenase is a regulatory enzyme of the oxidative pentose phosphate pathway in Schizasaccharomyces pombe. The enzyme is subject to negative cooperative regulation by D-glucose-6-phosphate as characterized by the Hill coefficient of 0.68 +/- 0.04. D-Glyceraldehyde-3-phosphate and D-ribulose-5-phosphate rectify the negative cooperativity as evidenced from a change in the Hill coefficients to 0.98 +/- 0.05 and 1.02 +/- 0.05, respectively. These pentose phosphate pathway intermediates also inhibit the enzyme competitively with respect to D-glucose-6-phosphate. Thus, D-glucose-6-phosphate dehydrogenase provides an avenue for regulating the partitioning of D-glucose between the redundant branches of the oxidative phosphate pathway in S. pombe.

Dose-Response Relationship, Drug↗

PubMed1978

Alterations of glucose metabolism during perfusion of rat lung with paraquat.

Isolated perfused rat lungs were used to investigate effects of paraquat on lung glucose metabolism. Lungs were ventilated with 5% CO2 in air and perfused with Krebs-Ringer bicarbonate buffer, pH 7.4, containing albumin and 5.5 mM radiolabeled D-glucose. Control lung glucose utilization, estimated from rate of 3H2O production from [5-3H]glucose, was 44 mumol/h-g dry wt. Pentose cycle activity, based on 14CO2 specific yields at the end of perfusions with [1-14C]- and [6-14C]glucose, was 14% of glucose utilization. During perfusion with 1.5 mM paraquat, glucose utilization increased 28%, 14CO2 production via the pentose cycle increased 182% (P less than 0.005), CO2 production via mitochondrial metabolism increased 39% (P less than 0.02), and the rate of lactate production increased 28% (P less than 0.05). Pyruvate production and the lactate-to-pyruvate ratio were not significantly altered. The data indicate that interaction of paraquat with the lung results in increased turnover of cytoplasmic NADPH and increased mitochondrial metabolism, but no significant change in cytoplasmic redox state. The findings are compatible with intracellular enzymatic reduction of paraquat by an NADPH-requiring reductase.

Animals↗

PubMed2000

Stimulation by iodide of H(2)O(2) generation in thyroid slices from several species.

The regulation of thyroid metabolism by iodide involves numerous inhibitory effects. However, in unstimulated dog thyroid slices, a small inconstant stimulatory effect of iodide on H(2)O(2) generation is observed. The only other stimulatory effect reported with iodide is on [1-(14)C]glucose oxidation, i.e., on the pentose phosphate pathway. Because we have recently demonstrated that the pentose phosphate pathway is controlled by H(2)O(2) generation, we study here the effect of iodide on basal H(2)O(2) generation in thyroid slices from several species. Our data show that in sheep, pig, bovine, and to a lesser extent dog thyroid, iodide had a stimulatory effect on H(2)O(2) generation. In horse and human thyroid, an inconstant effect was observed. We demonstrate in dogs that the stimulatory effect of iodide is greater in thyroids deprived of iodide, raising the possibility that differences in thyroid iodide pool may account, at least in part, for the differences between the different species studied. This represents the first demonstration of an activation by iodide of a specialized thyroid function. In comparison with conditions in which an inhibitory effect of iodide on H(2)O(2) generation is observed, the stimulating effect was observed for lower concentrations and for a shorter incubation time with iodide. Such a dual control of H(2)O(2) generation by iodide has the physiological interest of promoting an efficient oxidation of iodide when the substrate is provided to a deficient gland and of avoiding excessive oxidation of iodide and thus synthesis of thyroid hormones when it is in excess. The activation of H(2)O(2) generation may also explain the well described toxic effect of acute administration of iodide on iodine-depleted thyroids.

Animals↗

PubMed2002

Glutathione and K(+) channel remodeling in postinfarction rat heart.

Electrical remodeling of the diseased ventricle is characterized by downregulation of K(+) channels that control action potential repolarization. Recent studies suggest that this shift in electrophysiological phenotype involves oxidative stress and changes in intracellular glutathione (GSH), a key regulator of redox-sensitive cell functions. This study examined the role of GSH in regulating K(+) currents in ventricular myocytes from rat hearts 8 wk after myocardial infarction (MI). Colorimetric analysis of tissue extracts showed that endogenous GSH levels were significantly less in post-MI hearts compared with controls, which is indicative of oxidative stress. This change in GSH status correlated with significant decreases in activities of glutathione reductase and gamma-glutamylcysteine synthetase. Voltage-clamp studies of isolated myocytes from post-MI hearts demonstrated that downregulation of the transient outward K(+) current (I(to)) could be reversed by pretreatment with exogenous GSH or N-acetylcysteine, a precursor of GSH. Upregulation of I(to) was also elicited by dichloroacetate, which increases glycolytic flux through the GSH-related pentose pathway. This metabolic effect was blocked by inhibitors of glutathione reductase and the pentose pathway. These data indicate that oxidative stress-induced alteration in the GSH redox state plays an important role in I(to) channel remodeling and that GSH homeostasis is influenced by pathways of glucose metabolism.

Acetylcysteine↗

PubMed1989

Site of action of putative lipostatic factor: hypothalamic metabolism of parabiotic rats.

Studies were conducted to determine whether metabolic adaptation occurred in the hypothalamus of overfed parabiotic rats and their partners to distinguish between the adaptations caused by increased caloric intake and those caused by the production of a "lipostatic factor." The induction of overfed obesity in one parabiotic partner was employed to test the hypothesis that a putative lipostatic factor produced in the obese parabiotic elicited the hypophagic-lipid-mobilizing effect observed in the lean parabiotic via alterations in hypothalamic fatty acid and glucose metabolism. Fatty acid oxidation in the ventrolateral hypothalamus (VLH) of overfed parabiotic rats and their partners was lower than in ad libitum parabiotic rats. Net flux of glucose through the VLH gamma-aminobutyric acid (GABA) shunt was elevated in overfed parabiotic rats compared with the net flux observed in their partners and ad libitum parabiotic rats, the levels being similar in these last two groups. Net flux of glucose through the ventromedial hypothalamic (VMH) pentose shunt in overfed parabiotic rats and their partners was elevated relative to ad libitum parabiotic rats. The putative lipostatic factor may act to regulate energy balance through modification of VLH fatty acid oxidation and/or glucose flux via the VMH pentose shunt.

Animals↗

PubMed1979

Glucose metabolism in rat lung during exposure to hyperbaric O2.

Lung metabolism on exposure to hyperbaric oxygen was studied in rat lungs perfused with artificial media and ventilated with O2 at 0.2, 1, or 5 ATA. During the first 80 min of exposure to O2 at 5 ATA, glucose utilization increased 55%, lactate plus pyruvate production increased 45%, total CO2 production increased 47%, tissue ATP decreased 17%, and the ATP/ADP decreased 29% compared with 0.2 ATA O2. The increased CO2 production was due to a nearly twofold stimulation of pentose cycle activity whereas mitochondrial CO2 production did not change significantly. There were no significant differences in metabolism between lungs studied at 0.2 and 1 ATA O2. During the next hour of perfusion, there was a marked increase in mitochondrial CO2 production of control lungs but tissue ATP/ADP did not change significantly. With oxygen at 5 ATA, mitochondrial CO2 production increased only slightly, tissue ATP/ADP decreased further, and lungs demonstrated accumulation of edema fluid. The results indicate that exposure of lungs to hyperbaric oxygen results in stimulation of NADPH turnover through the pentose cycle and increased ATP generation, although the increased rate was not sufficient to maintain normal ATP/ADP.

Adenosine Triphosphate↗

PubMed1987

7-ethoxycoumarin O-deethylation in perfused livers from ethanol-fed rats: evidence for an important role of mitochondrial reducing equivalents.

Rates of 7-ethoxycoumarin (7EC) O-deethylation in perfused livers were increased approximately 3-fold by chronic ethanol feeding. The acute addition of ethanol (5 mM) and antimycin A (0.03 mM) strongly inhibited 7EC metabolism in perfused livers from ethanol-fed rats, but less inhibition was observed when these agents were added to microsomes or to perfused livers from control rats. The activity of the hepatic pentose phosphate cycle in perfused livers was assessed by comparing 14CO2 release during the infusion of 1-14C-glucose or 6-14C-glucose. 7EC infusion caused a 3-fold greater increase in 14CO2 production from 1-14C-glucose in a liver from a control rat than in a liver from an ethanol-fed rat, indicating greater hepatic pentose cycle activity in livers of control rats. Thus, the pronounced inhibition of 7EC metabolism caused by infusion of ethanol and antimycin A may be explained by a greater dependency on mitochondrial sources of NADPH in livers of ethanol-fed rats. Dinitrophenol (0.05 mM) did not inhibit 7EC metabolism in perfused livers, indicating that a reduction in the cellular redox state, and not diminished energetics, is involved in the mechanism of inhibition produced by antimycin A.

7-Alkoxycoumarin O-Dealkylase↗

PubMed1986

Red blood cell membrane lipid peroxidation in continuous ambulatory peritoneal dialysis patients.

We have recently described that in the erythrocytes from uremic patients on chronic hemodialysis, the pentose-phosphate shunt is defective, the membrane concentrations of malonyldialdehyde, resulting from peroxidation of polyunsaturated fatty acids in the membranes themselves, are increased, and the concentrations of vitamin E, an antioxidizing agent, are reduced. In the present study we have analyzed these same metabolic aspects in a group of uremic patients in continuous ambulatory peritoneal dialysis. We have found normal function of the pentose-phosphate shunt, slightly elevated concentrations of malonyldialdehyde compared to controls, but definitely lower than in chronic hemodialysis patients, and higher tocopherol concentrations than in both controls and chronic hemodialysis patients.

Adult↗

PubMed1975

Adipose tissue metabolism in essential fatty acid deficienty. Effects of prostaglandin e1, epinephrine, and ACTH.

In an effort to better define some of the metabolic changes that accompany essential fatty acid deficiency (EFAD), we studied glucose metabolism in adipose tissue of EFAD and normal mice under basal conditions and in the presence of prostaglandin E1 (PGE1), epinephrine, and ACTH1-18. Isolated fat cells were incubated in Krebs-Ringer bicarbonate medium containing glucose 1(-14C) or 6(-14C), and the incorporation of radioactive carbon into CO2, total fat, fatty acids, and glyceride-glycerol was determined. It was found that EFAD increased glucose uptake over controls which could be attributed to increased oxidation to CO2 and fatty acid synthesis. The contribution of the pentose cycle to glucose oxidation was 50-80% higher in EFAD adipocytes as compared to controls. ACTH1-18 (0.1 mug/ml) suppressed this by 18 and 30% in the control and EFAD groups, respectively, while epinephrine decreased pentose cycle activity by 83 and 55% in the two groups, respectively. PGE1 alone had no significant effect, but in combination with epinephrine it abolished the inhibitory action of the catecholamine in both groups. It is suggested that, although EFA serve as prostaglandin precursors, the effects of EFAD on the metabolism of fat cells cannot be reversed by PGE1, in vitro. However, these fat cells retain their responsiveness to the action of both lipolytic (ACTH and epinephrine) and antilipolytic (PGE1) agents.

Adipose Tissue↗

PubMed1982

Pathways of carbohydrate metabolism in peripheral nervous tissue. I. The contribution of alternative routes of glucose utilization in peripheral nerve and brain.

The activities of enzymes of the glycolytic route, the pentose phosphate pathway, the tricarboxylic acid cycle and lipogenesis have been measured in rat sciatic nerve and brain. Parallel studies have been made of the utilization of 14 C-labelled glucose and pyruvate in these two tissues. Comparison of the enzyme profiles and flux through alternative routes was based on activity relative to the rate of glucose phosphorylation as measured by the rate of formation of 3H2O from [2-3H]glucose. The contributions of the pentose phosphate pathway and lipogenesis to glucose utilization were substantially higher in sciatic nerve than brain. The relatively high activity of transketolase (EC 2.2.1.1) and transaldolase (EC 2.2.1.2) suggested a special role for these enzymes in sciatic nerve.

Animals↗

PubMed2003

Post-translational regulation of glucose-6-phosphate dehydrogenase activity in (pre)neoplastic lesions in rat liver.

Glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49) is the key regulatory enzyme of the pentose phosphate pathway and produces NADPH and riboses. In this study, the kinetic properties of G6PD activity were determined in situ in chemically induced hepatocellular carcinomas, and extralesional and control parenchyma in rat livers and were directly compared with those of the second NADPH-producing enzyme of the pentose phosphate pathway, phosphogluconate dehydrogenase (PGD). Distribution patterns of G6PD activity, protein, and mRNA levels were also compared to establish the regulation mechanisms of G6PD activity. In (pre)neoplastic lesions, the V(max) of G6PD was 150-fold higher and the K(m) for G6P was 10-fold higher than in control liver parenchyma, whereas in extralesional parenchyma, the V(max) was similar to that in normal parenchyma but the K(m) was fivefold lower. This means that virtual fluxes at physiological substrate concentrations are 20-fold higher in lesions and twofold higher in extralesional parenchyma than in normal parenchyma. The V(max) of PGD was fivefold higher in lesions than in normal and extralesional liver parenchyma, whereas the K(m) was not affected. Amounts of G6PD protein and mRNA were similar in lesions and in extralesional liver parenchyma. These results demonstrate that G6PD is strongly activated post-translationally in (pre)neoplastic lesions to produce NADPH.

Animals↗

PubMedDate not supplied

Enzymic pattern of preneoplastic and neoplastic lesions induced in the kidney of CBA mice by 1,2-dimethylhydrazine.

Mouse renal cell tumors (RCTs) were induced in male CBA mice by 5 subcutaneous injections of 8 mg 1,2-dimethylhydrazine (DMH)/kg body weight once a week. After a lag period of 2 yr kidneys were removed, and serial cryostat sections of the kidneys were histochemically analyzed for the following parameters: glycogen content, basophilia, and the activities of glycogen synthase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), glucose-6-phosphate dehydrogenase (G6PDH), hexokinase (HK), pyruvate kinase (PK), lactate dehydrogenase (LDH), malic enzyme (ME), succinate dehydrogenase (SDH), alkaline phosphatase (ALPase) and gamma-glutamyltranspeptidase (GGT). RCTs displayed the same histochemical profile irrespective of their size and growth pattern. In comparison with the normal kidney epithelium, the neoplastic cells exhibited elevated activities of enzymes for glycolysis (HK, PK, LDH) and the pentose phosphate pathway (G6PDH), while negative G6Pase and low SDH activity were observed in these cells. The majority of RCTs showed high PHO activity and weak staining for SYN. Activities of ALPase and GGT were negative in most of the RCTs. Markedly enlarged cells with atypical nuclei were detected in some advanced RCTs. Higher activities of glycolytic and mitochondrial enzymes and G6PDH were found in these enlarged cells than in other tumor cells. Tubular preneoplastic lesions were similar to neoplastic lesions in morphological and histochemical characteristics. The present study revealed that a markedly elevated capacity for glycolysis and the pentose phosphate pathway occurred in RCTs in mice. A similar histochemical pattern in the few preneoplastic tubular lesions observed suggests that these metabolic aberrations emerge early during carcinogenesis, but additional studies on early stages of renal carcinogenesis are needed to substantiate this assumption.

1,2-Dimethylhydrazine↗

PubMed2006

Metabolic network driven analysis of genome-wide transcription data from Aspergillus nidulans.

BACKGROUND: Aspergillus nidulans (the asexual form of Emericella nidulans) is a model organism for aspergilli, which are an important group of filamentous fungi that encompasses human and plant pathogens as well as industrial cell factories. Aspergilli have a highly diversified metabolism and, because of their medical, agricultural and biotechnological importance, it would be valuable to have an understanding of how their metabolism is regulated. We therefore conducted a genome-wide transcription analysis of A. nidulans grown on three different carbon sources (glucose, glycerol, and ethanol) with the objective of identifying global regulatory structures. Furthermore, we reconstructed the complete metabolic network of this organism, which resulted in linking 666 genes to metabolic functions, as well as assigning metabolic roles to 472 genes that were previously uncharacterized. RESULTS: Through combination of the reconstructed metabolic network and the transcription data, we identified subnetwork structures that pointed to coordinated regulation of genes that are involved in many different parts of the metabolism. Thus, for a shift from glucose to ethanol, we identified coordinated regulation of the complete pathway for oxidation of ethanol, as well as upregulation of gluconeogenesis and downregulation of glycolysis and the pentose phosphate pathway. Furthermore, on change in carbon source from glucose to ethanol, the cells shift from using the pentose phosphate pathway as the major source of NADPH (nicotinamide adenine dinucleotide phosphatase, reduced form) for biosynthesis to use of the malic enzyme. CONCLUSION: Our analysis indicates that some of the genes are regulated by common transcription factors, making it possible to establish new putative links between known transcription factors and genes through clustering.

Aspergillus nidulans↗

PubMed2005

Maillard reaction products derived from thiol compounds as inhibitors of enzymatic browning of fruits and vegetables: the structure-activity relationship.

Some thiol-derived Maillard reaction products (MRPs) may exert antioxidant activity, depending on the reaction conditions as well as on the sugar and the sulphydryl compound. Recently, we reported that MRPs derived from glucose or fructose with cysteine (CSH) or glutathione (GSH) mixtures greatly inhibited polyphenoloxidases (PPOs), oxidoreductases responsible for discoloration of fresh or minimally processed fruits and vegetables. Glucose and GSH were shown to be the most active in producing inhibitory MRPs. Therefore, we examined the way in which the nature of the reactants affected their synthesis, in order to establish a structure-activity relationship for the inhibitory products. Various aqueous (0.083 M, 0.125 M, or 0.25 M) mixtures of a sugar (hexose, pentose, or diholoside) with either a CSH-related compound (CSH, GSH, N-acetyl-cysteine, cysteamine, cysteic acid, methyl-cysteine, cysteine methyl ester), an amino acid (gamma-glutamic acid, glycine, methionine), or other sulfur compound (thiourea, 1,4-dithiothreitol, 2-mercaptoethanol) were heated at 103 degrees C for 14 h. Soluble MRPs were compared for their ability to inhibit apple PPO activity. In the presence of CSH, the rated sugars (same molar concentration) ranked as to inhibitory effect were pentoses > sucrose > hexoses > or = maltose. In the presence of glucose, the simultaneous presence of an amino group, a carboxyl group, and a free thiol group on the same molecule seemed essential for the production of highly inhibitory compounds.

Cysteine↗