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PubMed1997

The quaternary geometry of transcription termination factor rho: assignment by chemical cross-linking.

Transcription termination factor rho from Escherichia coli is a ring-shaped homohexamer of 419 amino acid subunits and catalyzes an ATP-dependent release of nascent RNA transcripts. Previous chemical cross-linking studies suggested that the rho hexamer might have D3 symmetry with three isologous dimers as protomers. However, our recent mutational analysis of rho alongside its putative structural homology to F1-ATPase rather argued for C6 symmetry. To resolve this discrepancy, we have re-investigated the pattern of cross-linking of rho using various cross-linkers with different functional groups and spacer lengths. Upon reaction with dimethyl suberimidate followed by SDS-polyacrylamide gel electrophoresis, rho protein generated a series of cross-linked oligomers up to hexamers, of which dimers migrated as distinct doublet bands of approximately equal intensities. However, the lower band became much stronger than the upper one with dimethyl adipimidate and difluorodinitrobenzene, and vice versa with disuccinimidyl glutarate, disuccinimidyl suberate and disulfosuccinimidyl tartarate. Furthermore, the trimeric products also produced doublet bands, whose relative intensities were again variable with cross-linkers, but in an inverse correlation with those of the dimer bands. These results combined with theoretical considerations support a C6 symmetry model in which cross-linking is assumed to occur stochastically at one of two alternative sites within each subunit interface with variable relative frequencies depending on cross-linkers. The D3 symmetry is excluded, for the putative trimeric subspecies should always retain mutually equal intensities in that case. Detailed inspections of the cross-linking kinetics further revealed a moderate characteristic of C3 symmetry for the rho hexamer such that the collective as well as relative rates of cross-linking at the two available sites could fluctuate between alternating interfaces. The final model designated as C3/6 is also compatible with other functional and structural properties known for rho.

Cross-Linking Reagents↗

PubMed1999

Assignment of electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO) to human chromosome 4q33 by fluorescence in situ hybridization and somatic cell hybridization.

Electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO) is a nuclear-encoded protein located in the inner mitochondrial membrane. Inherited defects of ETF-QO cause glutaric acidemia type II. We here describe the localization of the ETF-QO gene to human chromosome 4q33 by somatic cell hybridization and fluorescence in situ hybridization.

Animals↗

PubMed2002

Renal organic anion transport system: a mechanism for the basolateral uptake of mercury-thiol conjugates along the pars recta of the proximal tubule.

The basolateral handling of 20 microM inorganic mercury (Hg(2+)), in the form of mercuric conjugates of cysteine (Cys), N-acetylcysteine (NAC), or glutathione (GSH), was studied in isolated perfused S2 segments of the rabbit proximal tubule. One of the primary aims of the present study was to determine in a direct manner whether basolateral uptake of Hg(++) occurs in the pars recta of the proximal tubule and, more importantly, whether the p-aminohippurate-sensitive (PAH) organic anion transport system is involved in this process. Basolateral uptake and accumulation of Hg(++) occurred when the basolateral membrane of the tubular segments was exposed to mercuric conjugates of Cys, NAC, or GSH. Net basolateral uptake of Hg(++) was more than twice as great in the tubules exposed to mercuric conjugates of Cys or NAC than in the tubules exposed to mercuric conjugates of GSH, indicating that mercuric conjugates of Cys or NAC are transported more efficiently than mercuric conjugates of GSH. When PAH (1 mM) was added to the basolateral compartment (bath) surrounding a perfused S2 segment, the net uptake of Hg(++) (in the form of the mercuric conjugates) was reduced by 60-70%. In addition, when glutarate (4 mM), a transportable substrate for both the sodium-dependent dicarboxylate transporter and the dicarboxylate/organic anion exchanger (OAT1), was added to the basolateral compartment, there was a significant reduction in the uptake and accumulation of Hg(++) in the form of mercuric conjugates of Cys. Overall, these data indicate that Hg(++), in the form of biologically relevant mercuric conjugates of Cys, NAC, or GSH, is taken up significantly at the basolateral membrane of pars recta segments of the proximal tubule, and this uptake is mediated mainly by the actions of the PAH-sensitive organic anion transport system.

Acetylcysteine↗

PubMed1990

Genetic transformation of glutamine auxotrophy to prototrophy in the cyanobacterium Nostoc muscorum.

Glutamine auxotrophic (Gln-) and L-methionine D,L-sulfoximine (MSX) resistant (MSXr) mutants of N. muscorum were isolated and characterized for nitrogen nutrition, nitrogenase activity, glutamine synthetase (GS) activity and glutamine amide, alpha-keto-glutarate amido transferase (GOGAT) activity. The glutamine auxotroph was found to the GOGAT-containing GS-defective, incapable of growth with N2 or NH4+ but capable of growth with glutamine as nitrogen source, thus, suggesting GS to be the primary enzyme of both ammonia assimilation and glutamine formation in the cyanobacterium. The results of transformation and reversion studies suggests that glutamine auxotrophy is the result of a mutation in the gln A gene and that gln A gene can be transferred from one strain to another by transformation.

Ammonia↗

PubMed1976

Teratology study of two isoglutamine derivatives.

The embryotoxicity and teratogenicity of N-phthalyl isoglutamine (2), a metabolite of thalidomide, and of "K-2004-1c", 2-(bicyclo[2.2.1]heptane-2-endo-3-endo-dicarboximido)-glutaric acid 1-amide (4), the main metabolite of the test compound "K-2004" (proposed generic name: biglumide), a nonteratogenic congener of thalidomide, have been investigated in mice and rats. Whereas 2 proved to be highly teratogenic and embryotoxic, 4 showed none of these activities in the dose range from 50 to 400 mg/kg.

Abnormalities, Drug-Induced↗

PubMed1985

Transcription analysis of the sucAB, aceEF and lpd genes of Escherichia coli.

Transcript mapping of the Escherichia coli sucAB, aceEF and lpd genes, encoding the five components of the pyruvate and 2-oxoglutarate dehydrogenase complexes, was carried out using single-stranded M13 probes. The sucA and aceE genes encode the specific dehydrogenase components (E1o, E1p), and the sucB and aceF genes encode the specific dihydrolipoamide acyltransferases (E2o, E2p). The common lipoamide dehydrogenase (E3) component is encoded by a single lpd gene adjacent to the aceEF genes. The sucAB, aceEF and lpd genes were all expressed on independent transcripts, and the promoters and terminators were identified. In addition, readthrough transcription from the sucAB genes to a downstream gene designated sucC, and from the aceEF genes to the adjacent lpd gene, was found. The relative levels of transcription of the suc, ace and lpd genes, and of the three different transcript types covering the ace-lpd region, were quantified using RNA from cells grown on different substrates. Most of the E3 components supplying the pyruvate dehydrogenase complex appear to be synthesised from approximately 6415-base aceEF-lpd readthrough transcripts, but additional approximately 4640-base aceEF transcripts terminating after the aceF gene provide a transcriptional basis for the observed stoichiometric excess of E1p and E2p relative to E3 in the assembled complex. Conversely most of the E3 components required for the 2-oxo-glutarate dehydrogenase complex appear to be synthesised from the independent 1670-base lpd transcripts.

Acyltransferases↗

PubMed1983

Glutamic acid decarboxylase in Mycobacterium leprae.

Suspensions of Mycobacterium leprae purified from the organs (mostly spleen) of experimentally-infected armadillos (Dasypus novemcinctus, Linn) decarboxylated 1-(14C) glutamic acid liberating 14CO2. The reaction was pyridoxal phosphate-dependent and was inhibited by hydroxylamine, suggesting that it is a true amino acid decarboxylase. Loss of the activity at higher temperatures indicated the enzymatic nature of the reaction. Excess substrate or substrate analogs inhibited the decarboxylase whereas alpha-ketoglutarate and glutarate stimulated it. The activity was four times higher at pH 4.5 than at pH 6.8, suggesting that the enzyme is of microbial origin and not derived form the host cells. Armadillo spleen did not decarboxylate the amino acid. The Km value of the enzyme in the organisms was similar to that in Escherichia coli. The results reported here show that glutamate decarboxylase (EC 4.1.1.15) is an inherent metabolic activity of M. leprae, and might explain its unusual neural affinity. Glutamic acid is the most abundant amino acid occurring in the nerve tissue.

Carboxy-Lyases↗

PubMed1978

Nitrogen assimilation in Rhodopseudomonas acidophila.

Rhodopseudomonas acidophila strain 7050 assimilated ammonia via a constitutive glutamine synthetase/glutamate synthase enzyme system. Glutamine synthetase had a Km for NH+4 of 0.38 mM whilst the nicotinamide adenine dinucleotide linked glutamate synthase had a Km for glutamine of 0.55 mM. R. acidophila utilized only a limited range of amino acids as sole nitrogen sources: L-alanine, glutamine and asparagine. The bacterium did not grow on glutamate as sole nitrogen source and lacked glutamate dehydrogenase. When R. acidophila was grown on L-alanine as the sole nitrogen source in the absence of N2 low levels of a nicotinamide adenine dinucleotide linked L-alanine dehydrogenase were produced. It is concluded, therefore, that this reaction was not a significant route of ammonia assimilation in this bacterium except when glutamine synthetase was inhibited by methionine sulphoximine. In L-alanine grown cells the presence of an active alanine-glyoxylate aminotransferase and, on occasions, low levels of an alanine-oxaloacetate aminotransferase were detected. Alanine-2-oxo-glutarate aminotransferase could not be demonstrated in this bacterium.

Alanine↗

PubMed1983

Chronic elevation of brain GABA by gamma-vinyl GABA treatment does not alter the sensitivity of GABAergic or dopaminergic receptors in rat CNS.

Rat brain GABA levels were elevated chronically by daily administration of gamma-vinyl GABA, an enzyme-activated, irreversible inhibitor of GABA:2-oxo-glutarate aminotransferase (GABA-T; EC2.6.1.19). Following various periods of drug treatment and withdrawal, the sensitivity of dopamine and GABA receptors in the CNS was determined by biochemical and behavioral evaluations. In contrast to chronic haloperidol treatment, none of the treatment schedules with gamma-vinyl GABA had any significant effect on parameters such as apomorphine induced locomotor activity, [3H] spiperone binding or dopamine-stimulated adenylate cyclase in the corpus striatum; nor did gamma-vinyl GABA treatment affect [3H] GABA binding or GABA-activated [3H] diazepam binding in the cerebral cortex. Moreover, co-administration of gamma-vinyl GABA and haloperidol did not alter the ability of the neuroleptic to induce supersensitivity in the striatal dopaminergic system. Thus, it appears that, in contrast to reported studies using chronic administration of other less specific GABA-T inhibitors such as gamma-acetylenic GABA, amino-oxyacetic acid and isonicotinic acid hydrazide or direct GABA agonists such as THIP (4,5,6,7-tetrahydroisoxazolo (5,4-c-)-pyridin-3-ol) or kojic amine, gamma-vinyl GABA does not alter the sensitivity of the striatal dopaminergic system.

Adenylyl Cyclases↗

PubMed1988

3-Hydroxy-3-methylglutaryl-coenzyme A lyase deficiency: review of 18 reported patients.

3-Hydroxy-3-methylglutaryl-coenzyme A lyase deficiency (HMG-CoA lyase) is an inborn error of leucine catabolism which often leads to life-threatening illness in the neonatal period. The cardinal clinical features include severe infantile hypoglycemia, metabolic acidosis, hepatomegaly, lethargy or coma and apnea. Hyperammonemia is variable. There is a characteristic absence of ketosis. Considerable heterogeneity has been observed in clinical and biochemical presentation. Acute episodes of illness have been mistaken for Reye syndrome. The pattern of organic acids in the urine includes large amounts of 3-hydroxy-3-methylglutaric, 3-methyl-glutaconic, 3-methylglutaric and 3-hydroxyisovaleric acids. Smaller, but appreciable levels of glutaric, adipic and other dicarboxylic acids may also be excreted in the urine. Lactic acid may be present in sizable amounts at times of acute illness. The primary defect is a deficiency of 3-hydroxy-3-methylglutaryl-coenzyme A lyase, a key enzyme in the cycle of ketogenesis.

Amino Acid Metabolism, Inborn Errors↗

PubMed1982

3-hydroxy-3-methylglutaryl-CoA lyase deficiency in an infant with macrocephaly and mild metabolic acidosis.

A girl, now three years old, is reported, in whom at the age of 5 months the diagnosis of 3-HMG-CoA lyase deficiency was established. The characteristic excretion pattern consisted of 3-HMG, 3-CH3-glutaconic acid, 3-CH3-glutaric acid and 3-HIVA. Activity of 3-HMG-CoA lyase in leucocytes was very low. She had compensated metabolic acidosis and mild hypoglycemia. Therapy with a leucine restricted diet decreased excretion of metabolites moderately but did not influence the tendency to metabolic acidosis. Clinically the infant presented with macrocephaly. At the age of 3 years she is severely retarded. CAT scan revealed the picture of progressive demyelination of the white matter.

Acidosis↗

PubMed1986

Malonyl coenzyme A decarboxylase deficiency. Clinical and biochemical findings in a second child with a more severe enzyme defect.

A second child with a more severe deficiency of malonyl CoA decarboxylase is described. He is mildly mentally retarded and presented with vomiting, a seizure, hypoglycaemia and mild metabolic acidosis during a urinary tract infection. The urine contained increased amounts of malonic, methylmalonic, succinic, adipic, glutaric and suberic acids. Mitochondrial malonyl CoA decarboxylase activity in cultured fibroblast extracts was 4% of the mean control value. A high fat, low carbohydrate diet led to symptomatic hypoglycaemia, a moderate metabolic acidosis and excretion in the urine of large amounts of the same organic acids and 3-hydroxybutyrate. Only relatively small quantities of malonic, methylmalonic and succinic acid were excreted in the urine when the boy was fed an isocaloric low fat, high carbohydrate diet. Acute fat and lysine loads led to increased excretion of malonic acid in the urine without affecting the excretion of the other organic acids. Experience with this patient suggests that malonyl CoA decarboxylase serves an important function in the mitochondrion by preventing accumulation of malonyl CoA. The importance of the enzyme is best seen when fat is the main metabolic fuel. The mechanisms by which malonyl CoA produces its complex metabolic effects remain to be elucidated.

Acidosis↗

PubMed1977

[Azoindoxyl methods for the investigation of hydrolases. II. Biochemical and histochemical studies of acid beta-galactosidase (author's transl)].

The determination of various reaction constants yields the following assay for the photometric evaluation of acid beta-galactosidase (measurement of the azoindoxyl dye at 540 nm after extraction with dimethylformamide or -acetamide): 1.5 mM 5-Br-4-Cl-3-indolyl-beta-D-galactoside (1 mg dissolved in 0.05 ml dimethylformamide) and 0.01-0.015 ml hexazotized p-rosaniline/ml in 0.1 M citric acid-phosphate buffer, pH 4. By means of this procedure it becomes evident that the activity of the enzyme differs considerably in various rat organs; NaCl does not influence acid beta-galactosidase. -- Similar results were obtained with the indigogenic method; indigo can be dissolved and measured photometrically as the azoindoxyl dye. The enzyme is suppressed by high concentrations of hexazotized p-roaniline to 50%; low concentrations do not inhibit; the same is true for ferricyanide-ferrocyanide employed in the indigogenic media. -- The effect of glutar- and formaldehyde on acid beta-galactosidase cannot be investigated with the azoindoxyl reaction since the azoindoxyl dye partially withstands extraction from fixed blocks of tissue. On the basis of the biochemical findings the azoindoxyl technique can be recommended for the histochemical demonstration of acid beta-galactosidase: 7.5 mg (1.5 mM) 5-Br-4-Cl-3-indolyl-beta-D-galactoside (dissolved in 0.25 ml dimethylformamide) and 0.05-0.15 ml hexazonium-p-rosaniline in 10 ml 0.1 M citric acid-phosphate buffer, pH 4. After incubation the sections can be treated with osmium tetroxide followed by dehydration and mounting in resins or can be mounted without prior osmification of the azoindoxyl dye in glycerin jelly. The osmium chelate resists treatment with organic solvents; the stability of the chelate depends on the concentration of hexazotized p-rosaniline. After fixation in glutaraldehyde or in a mixture of form- and glutaraldehyde acid beta-galactosidase can be exactly localized in the lysosomes of many rat organs. In comparison with the indigogenic, the metal precipitation and the simultaneous azocoupling reactions for the in situ detection of acid beta-galactosidase the azoindoxyl procedure is superior if fixed material is used; it is equivalent or inferior in connection with membrane technique. The biochemical azoindoxyl assay represents a useful method for combined qualitative and quantitative studies of acid beta-galactosidase.

Aldehydes↗

PubMed1983

Reabsorption of dicarboxylic acids from the proximal convolution of rat kidney.

The transport of dicarboxylic acid in the late proximal convolution was investigated by measuring the 3.5 s efflux of 2-oxoglutarate from the tubular lumen of rats starved for 3 days. The 3.5 s efflux of 2-oxoglutarate comprises two components, one due to movement across the brush border, obeying Michaelis Menten kinetics with an apparent Km of 0.13 mmol/l and a Jmax of 0.41 pmol cm-1 s-1 and the other due to diffusional movement presumably via the paracellular pathway with a permeability of 23.0 microns2 s-1. Omission of sodium from the perfusion fluid reduced the transcellular efflux of 2-oxoglutarate by 76%, indicating a sodium-dependent transport system. Addition of 5 mmol/l lithium to the liminal and capillary perfusate reduced it by 56% indicating a specific inhibitory effect of lithium on dicarboxylic acid transport. Addition of 5 mmol/l H2DIDS to the luminal perfusate reduced 3.5 s transcellular 2-oxoglutarate efflux by 35%. The molecular specificity of the system was assessed by studying the inhibitory effects of a series of dicarboxylates, both aliphatic and aromatic, on the 3.5 s efflux of 2-oxoglutarate. Inhibitory constants (apparent Ki) were calculated for comparative purposes assuming competitive inhibition. From this, the system was found to have optimal affinity for dicarboxylates in the trans-configuration with a four or five carbon chain (i.e. succinate and glutarate). Substitution on the 2-carbon atom with CH3-, OH-, SH-, and O = resulted in little reduction in inhibitory potency as compared to succinate itself. However, 2-substitution with NH3+ (not with N-acetyl) as well as 2,3-disubstitution with CH3-, OH- or SH-, strongly reduced or abolished the inhibitory potency. Only with the exception of pyruvate all monocarboxylates tested, did not inhibit 2-oxoglutarate transport, but all tricarboxylates tested, i.e. citrate, isocitrate and tricarballate had an inhibitory effect. Citrate inhibition was higher at acidic than alkaline pH. A number of aromatic compounds was also tested. In most cases the inhibitory potency of the aromatic compounds was considerably weaker than that of the effective 4-5 carbon chain aliphatic compounds. Only benzene-1,4-dicarboxylate, benzene-2-nitro-1,4-dicarboxylate, and benzene-1,2-diacetate had a high inhibitory potency. In the case of the aromatic dicarboxylates the most important feature relating molecular structure to transport was the distance between the two carboxyl-groups in the molecule.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗

PubMed1989

Disorders of mitochondrial beta-oxidation: prenatal and early postnatal diagnosis and their relevance to Reye's syndrome and sudden infant death.

There are still many problems with the diagnosis and classification of inherited disorders of mitochondrial beta-oxidation. At present only the acyl-CoA dehydrogenase step of the beta-oxidation spiral has been explored in any detail and a large number of patients have disorders that cannot be properly characterized. beta-Oxidation defects may present in a wide variety of ways, the most dramatic being acute encephalopathy with hepatic involvement (atypical Reye's syndrome) or 'sudden' death. Investigations may include urinary and plasma organic acids, metabolic stress tests and assays of overall metabolic pathways or of specific enzymes in cultured fibroblasts, lymphocytes, or other material. Early postnatal diagnosis presents particular difficulties but in medium-chain acyl-CoA dehydrogenase deficiency the diagnosis may be apparent from careful examination of urine. There is as yet little general experience in prenatal diagnosis of this group of disorders except for glutaric aciduria type II. Single prenatal diagnoses of medium-chain acyl-CoA dehydrogenase deficiency and of an incompletely characterized defect of medium-chain fatty acid oxidation have been performed.

Acetyl Coenzyme A↗

PubMed1990

A comparison of [9,10-3H]palmitic and [9,10-3H]myristic acids for the detection of defects of fatty acid oxidation in intact cultured fibroblasts.

The production of tritiated water from [9,10-3H]myristic acid can be used as a screening assay for the detection of medium-chain acyl-CoA dehydrogenase deficiency, multiple acyl-CoA dehydrogenation defects (glutaric aciduria type 2 and ethylmalonic-adipic aciduria types), and some types of hydroxydicarboxylic aciduria. Comparison with the release of tritiated water from [9,10-3H]palmitic acid may give an indication of the chain-length specificity of the metabolic defect. In a case of ethylmalonic-adipic aciduria such a prediction has been confirmed by examination of accumulated intermediates in the affected fibroblasts.

Acyl-CoA Dehydrogenase↗

PubMed1985

Electrogenic calcium transport in plasma membrane of rat pancreatic acinar cells.

ATP-dependent 45Ca2+ uptake was investigated in purified plasma membranes from rat pancreatic acinar cells. Plasma membranes were purified by four subsequent precipitations with MgCl2 and characterized by marker enzyme distribution. When compared to the total homogenate, typical marker enzymes for the plasma membrane, (Na+,K+)-ATPase, basal adenylate cyclase and CCK-OP-stimulated adenylate cyclase were enriched by 43-fold, 44-fold, and 45-fold, respectively. The marker for the rough endoplasmic reticulum was decreased by fourfold compared to the total homogenate. Comparing plasma membranes with rough endoplasmic reticulum, Ca2+ uptake was maximal with 10 and 2 mumol/liter free Ca2+, and half-maximal with 0.9 and 0.5 mumol/liter free Ca2+. It was maximal at 3 and 0.2 mmol/liter free Mg2+ concentration, at an ATP concentration of 5 and 1 mmol/liter, respectively, and at pH 7 for both preparations. When Mg2+ was replaced by Mn2+ or Zn2+ ATP-dependent Ca2+ uptake was 63 and 11%, respectively, in plasma membranes; in rough endoplasmic reticulum only Mn2+ could replace Mg2+ for Ca2+ uptake by 20%. Other divalent cations such as Ba2+ and Sr2+ could not replace Mg2+ in Ca2+ uptake. Ca2+ uptake into plasma membranes was not enhanced by oxalate in contrast to Ca2+ uptake in rough endoplasmic reticulum which was stimulated by 7.3-fold. Both plasma membranes and rough endoplasmic reticulum showed cation and anion dependencies of Ca2+ uptake. The sequence was K+ greater than Rb+ greater than Na+ greater than Li+ greater than choline+ in plasma membranes and Rb+ greater than or equal to K+ greater than or equal to Na+ greater than Li+ greater than choline+ for rough endoplasmic reticulum. The anion sequence was Cl greater than or equal to Br greater than or equal to 1 greater than SCN greater than NO3 greater than isethionate greater than cyclamate greater than gluconate greater than SO2(4) greater than or equal to glutarate and Cl- greater than Br greater than gluconate greater than SO2(4) greater than NO3 greater than 1 greater than cyclamate greater than or equal to SCN, respectively. Ca2+ uptake into plasma membranes appeared to be electrogenic since it was stimulated by an inside-negative K+ and SCN diffusion potential and inhibited by an inside-positive diffusion potential. Ca2+ uptake into rough endoplasmic reticulum was not affected by diffusion potentials. We assume that the Ca2+ transport mechanism in plasma membranes as characterized in this study represents the extrusion system for Ca2+ from the cell that might be involved in the regulation of the cytosolic Ca2+ level.

Adenosine Triphosphate↗

PubMed1983

Metabolic changes in the rat liver during pregnancy. II. Tricarboxylic acid cycle.

During pregnancy the rat liver shows alterations in metabolism which apparently do not to occur in the non-pregnant animal. In our study, the following metabolite concentrations and enzyme activities in the liver of pregnant and non-pregnant rats were measured after fasting periods of 6 and 12 h: malate, fumarate, isocitrate, alpha-keto-glutarate, glutamate, malate-dehydrogenase, fumarate-hydratase, glutamate-dehydrogenase, isocitrate-dehydrogenase, aspartate-aminotransferase and after 12 h fast, the concentrations of acetyl coenzyme A and citrate. These results are discussed with regard to their possible importance for the maternal and fetal energy supply.

Animals↗