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PubMed1986

A probable new pathway for the biosynthesis of putrescine in Escherichia coli.

Some cultures of Escherichia coli BGA8, a mutant unable to synthesize putrescine, showed a change of behaviour and could grow almost equally well in either the absence or the presence of polyamines after repeated periods of polyamine starvation. Experiments in vivo with radioactive precursors showed that the bacteria which evaded the polyamine requirement had recovered their ability to synthesize putrescine from glucose or glutamic acid, but not from ornithine or arginine. These results are in agreement with the fact that the polyamine-independent cells were still deficient in the enzymes ornithine decarboxylase and agmatinase. Our findings seem to indicate the existence of a new pathway synthesize putrescine which does not involve ornithine or arginine as intermediates.

Arginine↗
PubMed1989

Inhibition by a nonmetabolized analogue of L-leucine of protein biosynthesis in tumoral pancreatic islet cells.

The effect of L-leucine, its deaminated metabolite 2-ketoisocaproate and its nonmetabolized analogue b(+/-)2-aminobicyclo[2,2,1]-heptane-2-carboxylic acid (BCH) upon protein labelling was examined in tumoral islet cells (RINm5F line) exposed to L-[4-3H]phenylalanine or L-[3-3H]serine. The interpretation of the results, in terms of changes in biosynthetic activity, was obscured by a possible interference of the tested nutrients with the uptake and further metabolism of the tracer tritiated amino acids. Nevertheless, when the cells were preincubated with the nutrient secretagogues and then incubated in the sole presence of L-[3-3H]serine, BCH, but not L-leucine or 2-ketoisocaproate, still inhibited protein labelling, this coinciding with a decrease in the ratio between TCA-precipitable and total radioactivity in the RINm5F cells. The inhibitory action of BCH was antagonized, to a limited extent, by D-glucose. It is proposed that BCH could be used as a tool to interfere with the function and growth of insulinoma cells.

Adenoma, Islet Cell↗
PubMed1979

Biodegradation of 1,2,3- and 1,2,4-trichlorobenzene in soil and in liquid enrichment culture.

The biodegradation of radiochemically pure (99%) 1,2,3- and 1,2,4-trichlorobenzene (TCB) in soil was investigated. Experimental difficulties posed by the high volatility and slow biodegradation rate of the TCBs were partially overcome by using a specially designed incubation and trapping apparatus. Evolution of (14)CO(2) from active versus poisoned soil dosed with 50 mug of the individual TCBs per g gave conclusive proof that both isomers are biodegradable. At 20 degrees C, 1,2,4-TCB was mineralized at an approximate rate of 1 nmol/day per 20 g of soil sample, and 1,2,3-TCB was mineralized at one-half to one-third that rate. Mineral fertilizers or cosubstrates failed to increase TCB mineralization rates in soil. Anaerobic conditions had a negative effect on mineralization, and increased temperatures had a positive effect. With increasing 1,2,4-TCB concentrations, (14)CO(2) evolution exhibited saturation kinetics with an apparent K(m) of 55.5 nmol per g of soil. Recovery of total radioactivity was good from soil containing high organic matter concentrations. From low-organic-matter soil, some of the radioactivity was recovered only on combustion, and overall recovery was lower. In soil-inoculated liquid culture, the cosubstrates glucose and benzene caused a slight stimulation of 1,2,4-TCB mineralization. Cochromatography of known standards with the extracts of soil pretreated with [(14)C]TCBs indicated that 3,4,5-trichlorophenol, 2,6-dichlorophenol and, to a lesser degree, 2,3-dichlorophenol were present in soils incubated with 1,2,3-TCB. 2,4-, 2,5-, and 3,4-dichlorophenol were present in soils incubated with 1,2,4-TCB.

Bacteria↗
PubMed1976

Properties of an inducible uptake system for beta-ketoadipate in Pseudomonas putida.

Wild-type strains of Pseudomonas putida form an inducible uptake system that appears to act on beta-ketoadipate under normal physiological conditions. The system is induced by beta-ketoadipate and is represented by catabolites derived from it. Adipate is metabolized very slowly by wild-type P. putida cultures; [14C]adipate was used as an analogue of beta-ketoadipate to measure the transport activity in wild-type cells and in cells that constitutively produced the uptake system. Constitutive cells that contained high levels of the uptake system concentrated adipate to a level up to 200-fold above the concentration in the external medium. The process was energy dependent. The activity of the system with radioactive adipate was inhibited by beta-ketoadipate, by beta-ketoadipate analogues, and by some compounds (e.g., acetate, glucose) that are structurally unrelated to beta-ketoadipate; it is not known if the inhibitory effects are exerted directly by the compounds themselves or indirectly by catabolites derived from the compounds. The discovery of the beta-ketoadipate uptake system is surprising in view of earlier studies that had indicated that beta-ketoadipate does not permeate the membrane of wild-type P. putida cells. Contradictions between the former investigations and the present analysis are due primarily to the relatively high concentrations of substrate used in the earlier experiments. The existence of the beta-ketoadipate uptake system indicates that beta-ketoadipate may exist as a selective nutrient in the natural niche of P. putida and may play a determinative role in the evolution of induction mechanisms that are characteristic of fluorescent pseudomonads.

Adipates↗
PubMed1991

The effect of carbohydrates in milk on the absorption of calcium by postmenopausal women.

The purpose of this investigation was to determine if the presence of carbohydrate in milk, either lactose or its hydrolysis products, enhance the bioavailability of calcium (Ca) in milk. Two studies were performed. In study A, fractional Ca absorption was measured in 11 lactose-tolerant postmenopausal women after an oral dose of 47Ca-equilibrated milk formula containing no carbohydrate (NOCHO), lactose (LACTOSE), or an equivalent amount of glucose plus galactose (SUGAR); all participated in three absorption studies in random order. The NOCHO formula contained 10.0 g protein and 217 mg Ca from a combination of milk mineral and protein isolates; the LACTOSE and SUGAR formulae contained in addition 12 g lactose or 6 g glucose plus 6 g galactose, respectively. In study B, fractional Ca absorption was measured in five postmenopausal women after an oral dose of 47Ca-equilibrated skim milk (217 mg Ca) and lactase-treated milk, each with sufficient carbohydrate added to equal 12 g. For both studies, the increase in forearm radioactivity 4 and 8 hours after oral 47Ca administration relative to the increase observed after IV administration was used to estimate fractional Ca absorption. The addition of lactose but not glucose plus galactose to the NOCHO formula enhanced Ca absorption (p less than 0.05). Fractional absorption at 4 hours was 0.386 from the LACTOSE formula compared with 0.310 for both the NOCHO and SUGAR formulae. Those individuals with the lowest absorption in the absence of carbohydrate had the greatest increase with lactose. In contrast, Ca absorption was the same from skim milk as from lactase-treated skim milk (study B).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

75,77Br- and 123I-analogues of D-glucose as potential tracers for glucose utilisation in heart and brain.

A number of D-glucose analogues labelled with either the positron emitter 75Br (T 1/2 = 1.6 h) or the single photon emitter 123I (T 1/2 = 13.3 h) were studied as potential tracers for glucose utilisation in heart and brain. Of these, 3-deoxy-3-bromo-D-glucose, 3-deoxy-3-iodo-D-glucose, methyl 2-deoxy-2-bromo-beta-D-glucoside and methyl 2-deoxy-2-iodo-beta-D-glucoside showed little uptake of radioactivity into brain and an unfavourable ratio of heart-to-blood and heart-to-lung concentrations. In contrast, methyl 3,4,6-tri-O-acetyl-2-deoxy-2-iodo-beta-D-glucoside (MTIG) and methyl 3,4,6-tri-O-acetyl-2-deoxy-2-bromo-beta-D-glucoside (MTBG) showed promising brain uptake (160% MBC for MTBG) with a good brain-to-blood concentration ratio of 0.8. MTBG is not metabolically altered in the brain. Thus, this compound may be a promising tracer for measuring glucose transport if it proves to be a substrate for the hexose carrier at the blood-brain-barrier.

Animals↗
PubMed1970

Electron microscope radioautographic study of glycogen synthesis in the rabbit retina.

Glycogen is present in the rabbit retina in monoparticulate form. Beta particles ( approximately 229 A) are abundant in Müller cell cytoplasm, particularly in its inner portion, decreasing in number outwards along the cell. They are slightly larger ( approximately 250 A) and much scarcer in neurons, though regularly present in the juxtanuclear Golgi region of ganglion cells. When the retina was incubated in a glucose-free medium, it was rapidly depleted of native glycogen. On further incubation in medium containing glucose-(3)H plus unlabeled glucose, glycogen reappeared in the form of beta particles of the same size and distribution as native ones, while radioautography revealed the appearance of amylase-labile radioactivity in the same locations. This newly formed glycogen was not associated with any particular organelle. The rate of synthesis, as judged from the amount of radioactivity, was high in the inner portion of Müller cells and declined uniformly toward the cell outer end, following a logarithmic gradient. The rate of synthesis was low in ganglion cells, at best approaching values in the outer portion of Müller cells. The concentration of glycogen in the inner portion of Müller cells is consistent with the view that it may be the source of glucose for the anaerobic glycolysis prevailing in the inner retina.

Animals↗
PubMed2003

Pharmacokinetics and metabolism of a COX-2 inhibitor, valdecoxib, in mice.

The pharmacokinetics and metabolism of valdecoxib, a potent cyclooxygenase-2 selective inhibitor, were investigated in mice. Valdecoxib was extensively metabolized after a single 5 mg/kg oral administration of [(14)C]valdecoxib and elimination of unchanged drug was minor (less than 1%) in male and female mice. The total mean percentage of administered radioactive dose recovered was 99.8% in the male mice and 94.7% in the female mice. Sixteen metabolites were identified in mouse plasma, red blood cells, urine, and feces. The main phase I metabolic pathway of valdecoxib in mice involved the oxidation of the 5-methyl group to form the active hydroxymethyl metabolite M1. M1 was further oxidized to the carboxylic acid metabolite M4, which underwent opening of the isoxazole ring to form M6 and M13. Phase II metabolism included glucuronide, glucoside, and methyl sulfone conjugations. M1 was also conjugated with glucuronic acid and glucose to yield M-G and M1-glucose, respectively. Three novel methylsulfone conjugates M20, M21, and M21-G were detected in blood or urine. Valdecoxib and M1 were the major radioactive components in plasma and red blood cells. The plasma area under the curve from zero to infinity (AUC(0-infinity)) values for valdecoxib and M1 were 3.58 and 0.850 microg. h/ml in males and 2.08 and 1.63 microg. h/ml in females, respectively. The RBC AUC(0-infinity) values for valdecoxib and M1 were 12.1 and 22.6 microg. h/g in males and 6.42 and 35.2 microg. h/g in females, respectively.

Animals↗
PubMedDate not supplied

Incorporation of radiolabelled sugars into synaptic junctional macromolecules from chick brain.

Individual radiolabelled sugars ([1-14C]-L-fucose, [U-14C]-D-galactose, [U-14C]-D-mannose, [U-14C]-D-glucose and [U-14C]-D-glucosamine) were injected intraventricularly into the forebrains of day-old chickens, and the relative incorporation, after 6 hr, into the glycoprotein sugars, aglycosyl protein, glycolipid sugars and aglycosyl lipid assessed. In addition, the relative total and specific activities of the individual glycoprotein sugars was also determined. Exclusive labelling of glycoprotein sugars (and of the fucose within these oligosaccharides) using fucose as precursor was confirmed, while optimal labelling of glycolipid sugars was achieved using the precursor mannose. Galactose, mannose, glucose and glucosamine were converted to varying degrees to other sugars and non-sugar precursors prior to incorporation. Glucosamine gave rise to the most even distribution of radioactivity among the glycoprotein sugar residues. The highest relative specific activities of the glycoprotein oligosaccharides were achieved using fucose and glucosamine as precursors.

Acetylgalactosamine↗
PubMedDate not supplied

Methylmercury induced biochemical and microsomal changes in the rat liver.

The change in the levels of DNA, RNA, protein, glucose-6-phosphatase, and microsomal enzymes in the rat liver following exposure to methylmercury was studied. The turnover rate of the membranes was also investigated by means of radioactive glycerol. A marked increase in microsomal enzyme levels, with no increase in smooth endoplasmic reticulum, was found one to four hours following administration. A delay in incorporation of radioactive glycerol and more rapid degradation of microsomal membranes were also detected as a result of mercury intoxication. These observations suggest an instability of the microsomal membranes which would be responsible for the early increase in microsomal enzymes upon homogenization. A general inhibition of the microsomal enzymes and proteins was found 1-2 days after mercury administration. The inhibition of glucose-6-phosphatase activity, however, was not noted until day 5. Most of the enzymatic activities returned to normal between days 5 and 8. A reduction of DNA and protein was found in the liver homogenate after 2 hours of intoxication. However, no change in the RNA level was detected.

Animals↗
PubMed1998

[Identification of the ischemic origin of dilated myocardiopathy using positron emission tomography].

INTRODUCTION AND OBJECTIVES: The aim of this study was to differentiate ischemic from nonischemic dilated cardiomyopathy with positron emission tomography. This differentiation is necessary to establish an adequate treatment, and it is often difficult with non-invasive diagnostic procedures. METHODS: Ten patients with an echocardiographic diagnosis of dilated cardiomyopathy who had undergone coronary angiography were selected. The presence or absence of angiographic coronary lesions was used to define the ischemic (n = 6) and the nonischemic group (n = 4). The ejection fraction was depressed in both groups, with no significant differences found. A perfusion study with 13N-ammonium and a metabolic imaging with 18F-florodeoxyglucose were performed on each patient. The images were quantitatively and qualitatively analysed, defining three criteria: accumulation defect (areas with activity under 50% of the maximal radioactivity), degree of heterogeneity, and match of images with both tracers. To determinate the degree of heterogeneity, nine segments on the three standard tomographic planes were studied. Based on the following heterogeneity features: irregular borders, coexisting different degrees of accumulation, and patched accumulation, a score ranging from 0 to 3 points was assigned to these segments. To analyse the radioactivity defects and the matching of studies with both tracers, the accumulation defects or the accumulating surface were outlined on a midventricular level coronal plane. RESULTS: The ischemic group has contrary to the nonischemic one, wider perfusion (0.26 +/- 0.21 vs 0.00) and metabolism defects (0.38 +/- 0.30 vs 0.06 +/- 0.09; p < 0.05). The degree of heterogeneity is significantly higher in the nonischemic group, either in perfusion (14.5 +/- 8.38 vs 2.5 +/- 1.04; p < 0.05) or in metabolism studies (15.5 +/- 3.31 vs 2.33 +/- 1.50; p < 0.005). Assigning wide defects and homogeneous accumulation to ischemic cardiomyopathy, and absence of defects and heterogeneous accumulation to nonischemic cardiomyopathy, the aetiology of the disease was identified in 9 of the 10 cases in the perfusion study and 100% of them with the metabolism imaging. CONCLUSIONS: Positron emission tomography allows to identify the aetiology of dilated cardiomyopathy, either with coronary perfusion or with myocardial glucose metabolism studies. Thus, only one of both PET studies could be used. Ischemic cardiomyopathy is characterised by wide defects and homogeneous radioactivity, and the nonischemic one by the absence of defects and heterogeneous accumulation of the tracer.

Aged↗
PubMed1985

Effects of ganglioside GM1 treatment on striatal glucose metabolism, blood flow, and protein phosphorylation of the rat.

Effects of ganglioside GM1 administration have been studied in unilaterally partially hemitransected rats on striatal energy metabolism, using the radioactive deoxyglucose (DG) technique, on striatal blood flow, using radiolabelled iodoantipyrine (IAP) as tracer, and on cyclic AMP (cAMP) and Ca2+ induced protein phosphorylation in striatal membranes (P2 fraction). Ganglioside GM1 treatment counteracted the imbalance in striatal energy metabolism, in striatal blood flow, as well as in protein phosphorylation found between the striata of the lesioned and unlesioned side, possibly due to excitatory effects on the lesioned side and inhibitory effects on the unlesioned side. In intact animals, GM1 treatment produced a reduction in cAMP and Ca2+ induced striatal protein phosphorylation. Facilitatory actions of the ganglioside GM1 dominate following a lesion, probably due to its possible function as a modulator of receptors for neuronotrophic factors, leading to restoration of metabolic rate and of cAMP and Ca2+ induced protein phosphorylation in the striatum of the lesioned side. The results emphasize that ganglioside GM1 treatment can restore the metabolism of a partially innervated striatum towards normal, as evaluated both at the level of the entire striatal structure by means of the DG and IAP techniques and at the molecular level by means of studies on the cAMP and Ca2+ induced protein phosphorylation.

Animals↗
PubMed1986

Covalent modification of substrate-binding sites of Escherichia coli ADP-glucose synthetase. Isolation and structural characterization of 8-azido-ADP-glucose-incorporated peptides.

A photoaffinity substrate analogue, 8-azido-ADP-[14C]glucose, reacts specifically and covalently with Escherichia coli ADP-glucose synthetase. The site(s) of reaction of 8-azido-ADP-[14C]glucose with the enzyme was identified by isolation of tryptic peptides containing the labeled analogue by use of high performance liquid chromatography technique and subsequent NH2-terminal sequence analysis of the purified radioactive peptides. One major binding region of the azido analogue is a peptide segment composed of residues 107-114 of the enzyme's polypeptide chain. Lys 108 and Arg 114 become trypsin-resistant sites when the enzyme is photoinactivated by 8-azido-ADP-[14C] glucose, suggesting that the analogue binds at or near the vicinity of these 2 basic amino acid residues. Conformational analysis of this peptide segment (residues 107-114) shows a strong probability of a reverse beta-turn secondary structure, suggesting that this peptide segment is on the enzyme surface. Two minor reaction regions of the enzyme with the analogue were also identified by chemical characterization. One region was composed of residues 162-207. Lys 194 was previously suggested as the activator-binding site by chemical modification studies with pyridoxal phosphate (Parsons, T. F., and Preiss, J. (1978) J. Biol. Chem. 253, 7638-7645). Another minor region where the analogue binds the tryptic peptide composed of residues 380-385 is near the COOH-terminal side of the enzyme. It is postulated that all these peptide segments are juxtaposed in tertiary structure.

Adenosine Diphosphate↗
PubMed1976

Metabolism of maltose in perfused rat liver and in isolated hepatocytes.

The conversion of 14C-maltose into glucose, lactate and 14 CO2 was studied in perfused livers from fed and fasted rats and in isolated hepatocytes. Maximal glucose production was 30 mM x g-1 x h-1; half-maximal rates were found with 3 mM maltose. About 0.01 % of the radioactivity infused was recovered as 14CO2. The addition of maltose had no effect on rates of oxygen consumption, lactate production or ketogenesis. The data suggest that maltose did not serve as a major substrate for biosynthetic or energy producing processes under the conditions of the perfused rat liver.

Animals↗
PubMed1998

Effects of FFA on insulin-stimulated glucose fluxes and muscle glycogen synthase activity in rats.

To examine effects of free fatty acids (FFA) on insulin-stimulated glucose fluxes, euglycemic hyperinsulinemic (86 pmol . kg-1 . min-1) clamps were performed for 5 h in conscious rats with (n = 8) or without (n = 8) lipid-heparin infusion. Glucose infusion rate required to maintain euglycemia was not different between the two groups during the first 2 h of clamps but became significantly lower with lipid-heparin infusion in the 3rd h and thereafter. To investigate changes in intracellular glucose metabolism during lipid-heparin infusion, additional clamps (n = 8 each) were performed for 1, 2, 3, or 5 h with an infusion of [3-3H]glucose. Insulin-stimulated whole body glucose utilization (Rd), glycolysis, and glycogen synthesis were estimated on the basis of tracer concentrations in plasma during the final 40 min of each clamp. Similar to changes in glucose infusion rate, Rd was not different between the two groups in the 1st and 2nd h but was significantly lower with lipid-heparin infusion in the 3rd h and thereafter. Whole body glycolysis was significantly lower with lipid-heparin infusion in all time periods, i.e., 1st, 2nd, 3rd, and 5th h of clamps. In contrast, whole body glycogen synthesis was higher with lipid-heparin infusion in the 1st and 2nd h but lower in the 5th h. Similarly, accumulation of [3H]glycogen radioactivity in muscle glycogen was significantly higher with lipid-heparin during the 1st and 2nd h but lower during the 3rd and 5th h. Glucose 6-phosphate (G-6-P) concentrations in gastrocnemius muscles were significantly higher with lipid-heparin infusion throughout the clamps. Muscle glycogen synthase (GS) activity was not altered with lipid-heparin infusion at 1, 2, and 3 h but was significantly lower at 5 h. Thus increased availability of FFA significantly reduced whole body glycolysis, but compensatory increase in skeletal muscle glycogen synthesis in association with accumulation of G-6-P masked this effect, and Rd was not affected in the early phase (within 2 h) of lipid-heparin infusion. Rd was reduced in the later phase (>2 h) of lipid-heparin infusion, when glycogen synthesis was reduced in association with reduced skeletal muscle GS activity.

Analysis of Variance↗
PubMed1986

Mathematical model of the metabolism of 123I-16-iodo-9-hexadecenoic acid in an isolated rat heart. Validation by comparison with experimental measurements.

The aim of the present study was to demonstrate that it is possible to estimate the intracellular metabolism of a fatty acid labelled with iodine using external radioactivity measurements. 123I-16-iodo-9-hexadecenoic acid (IHA) was injected close to the coronary arteries of isolated rat hearts perfused according to the Langendorff technique. The time course of the cardiac radioactivity was measured using an INa crystal coupled to an analyser. The obtained curves were analysed using a four-compartment mathematical model, with the compartments corresponding to the vascular-IHA (O), intramyocardial free-IHA (1), esterified-IHA (2) and iodide (3) pools. Curve analysis using this model demonstrated that, as compared to substrate-free perfusion, the presence of glucose (11 mM) increased IHA storage and decreased its oxidation. These changes were enhanced by the presence of insulin. A comparison of these results with measurements of the radioactivity levels within the various cellular fractions validated our proposed mathematical model. Thus, using only a mathematical analysis of a cardiac time-activity curve, it is possible to obtain quantitative information about IHA distribution in the different intracellular metabolic pathways. This technique is potentially useful for the study of metabolic effects of ischaemia or anoxia, as well as for the study of the influence of various substrates or drugs on IHA metabolism in isolated rat hearts.

Animals↗
PubMed1975

Covalently bound FAD in d-6-hydroxynicotine oxidase. Immunological studies of D- and L-6-hydroxynicotine oxidase: evidence for a D-enzyme precursor.

Antersera prepared against both enantiozymes, D- and L-6-hydroxynicotine oxidase, formed precipitins in double diffusion tests with their respective antigens only. A mixture of the two antisera caused spur formation of the two precipitin lines obtained with the pure enzymes. Antiserum to L-apoprotein reacted with native L-enzyme and L-apoprotein but not with the D-sspecific enzyme. D-6-hydroxynicotine oxidase activity was inhibited by the anti-D-antiserum, leaving the L-enzyme fully active, while anti-L-antiserum inhibited the L- but not the D-specific activity. The delayed induction of D-6-hydroxynicotine oxidase as compared to the other activities of the nicotine-degrading sequence and the differential immunochemical behavior of the enantiozymes allowed the search for a D-enzyme precursor. In cells harvested 3 hours after the addition of DL-nicotine, the L-enzyme activity was present, whereas no D-enzyme activity could be detected. However, an extract of these cells did form an immunoprecipitin line with anti-D-antiserum. L-6-Hydroxynicotine oxidase, but no D-6-hydroxynicotine oxidase activity, could also be induced in Arthrobacter oxidans grown in a medium with a high glucose content and DL-nicotine as the sole nitrogen source. An extract of these L-induced cells produced the specific immunoprecipitation with anti-D-antiserum. A pulse-chase experiment with cells grown first on glucose and DL-nicotine in the presence of [14C]leucine and then in an unlabeled medium which induces D-6-hydroxynicotine oxidase activity resulted in a radioactive D-enzyme-immunoprecipitin line. From these experiments it is concluded that a precursor of the active D-enzyme is induced simultaneously with the other nicotine-degrading enzymes.

Arthrobacter↗