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At least 19 recordsLinked to original sources
PubMed1975

Assimilation of citric acid and adipic acid by the blue-green alga Anabaena variabilis.

The assimilation of [1,6-14C] citric acid and [1,6-14C] adipic acid by the blue-green alga Anabaena variabius was studied in the dark and in the light. Citric acid was assimilated in the dark and in the light but adipic acid showed only limited assimilation in the dark. In the light the assimilation of adipic acid did not enhance the growth of the alga at a concentration of 2.85 X 10(-8) M. Growth was inhibited at adipic acid concentrations greater than 10(-3) M. Analysis of the products of adipic acid metabolism showed the presence of aspartic acid, glutamic acid, leucine, proline, and threonine and threonine amongst other unidentified compounds. A mechanism of beta-oxidation is proposed.

Adipates↗
PubMed1979

Gas-liquid chromatographic determination of adipic acid in crackling candy and soft drinks.

A procedure was developed for the simple and rapid determination of adipic acid in crackling candy and also in soft drinks. An alkaline solution of sample was extracted with ethyl ether to remove fatty substances, and H2SO4 was added to water layer to adjust the pH to less than 2. The acidified layer was saturated with NaCl and then extracted with ether. After drying, the ether layer was concentrated and the adipic acid in the concentrate was methylated using the diazomethane methograph equipped with a flame ionization detector. Recovery of adipic acid from crackling candy and from 2 kinds of soft drinks that had been fortified at the 200 ppm level was 96%. An interlaboratory test was carried out on the determination of adipic acid in orange soft drink. The results obtained by 6 laboratories were between 91 and 100% compared with the theoretical value.

Adipates↗
PubMed1976

Separation of myosin subfragment-1 into fractions containing g1 chani and g2 chain by Sepharose-adipic acid hydrazide-ATP column chromatography.

Subfragment-1 prepared by chymotryptic digestion of myosin was applied to a column of Sepharose-adipic acid hydrazide-ATP in 1 mM EDTA, 10 mM Tris-HCL (PH 7.6), and 40 mM KCL. Ninety-nine per cent of subfragment-1 was adsorbed on the column in this medium. Fourty-three per cent of the applied protein was eluted with 6 mM ADP in the above buffer and then 52% was eluted with 1 mM EDTA, 10 mM Tris-HCL (pH 7.6), AND 0.7 M KCL. The former fraction contained g3 chain and the latter g1 chain. These fractions were apparently the same as the components, p2 and p1, respectively, isolated by ion-exchange chromatography using DEAE-cellulose (Yagi & Otani (1974) J. Biochem. 76, 365-373). No significant difference of ADP binding was found between the two fractions, both could bind about 0.5 mole per 10(5) g of protein. The preparation of the two subfragment-1 fractions is described.

Adenosine Diphosphate↗
PubMed1979

Ethylmalonic-adipic aciduria. In vivo and in vitro studies indicating deficiency of activities of multiple acyl-CoA dehydrogenases.

The mechanisms underlying ethylmalonic-adipic aciduria were studied in a 5-yr-old girl. Oxidation of radioactive substrates by cultured skin fibroblasts from the proband and asymptomatic family members was also determined and compared to that by normal fibroblasts and that by cells from a patient with glutaric aciduria type II. Feeding medium-chain triglycerides promptly induced vomiting and lethargy accompanied by a pronounced increase of urinary ethylmalonate. Significant increases of serum isovalerate and urinary isovalerylglycine were observed after leucine feeding, but urinary glutarate increased only slightly after lysine feeding. Thus, the results from clinical investigation remained equivocal as to whether pathways other than fatty acid oxidation were blocked in our patient. Oxidation of [1-(14)C]butyrate by cultured skin fibroblasts from the proband was reduced to 14% of control. In vitro oxidation of [2-(14)C]lysine and [2-(14)C]leucine was also reduced to 28 and 23% of control, respectively. Much more severe reduction in oxidation of these three substrates (3, 9, and 9%, respectively) was observed in glutaric aciduria type II cells. These results indicated that in the proband, degradative pathways of fatty acids, lysine, and leucine are blocked at the steps of butyryl-CoA, glutaryl-CoA, and isovaleryl-CoA dehydrogenases, respectively, as in the case of glutaric aciduria type II. Because activities of multiple acyl-CoA dehydrogenases are reduced, a deficiency of electron-transferring flavoprotein, which serves as a hydrogen-acceptor for these dehydrogenases, is postulated as the underlying mechanisms of these two diseases, but a genetic heterogeneity was indicated by significant differences in the residual activities in these two types of cells. The hypothesis of more than one mutant allele of an autosomal recessive gene was also suggested by the study on cells from asymptomatic members of the family.

Acidosis↗
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↗
PubMed1979

Pattern of aliphatic dicarboxylic acids in uremic serum including a new organic acid, 2,4-dimethyladipic acid.

(1) 2,4-Dimethyladipic acid was first identified in normal human urine using gas chromatography-mass spectrometry. Urinary excretion of 2,4-dimethyladipic acid in 7 healthy adults ranged from 4.9 mumol to 14 mumol per 24 h. (2) Succinic acid, adipic acid, 3-methyladipic acid, 2,4-dimethyladipic acid, pimelic acid and azelaic acid were identified in the ultrafiltrate of the blood obtained from a chronic uremic patient using a hemodialyzer. (3) Levels of succinic acid, adipic acid, 3-methyladipic acid, 2,4-dimethyladipic acid, pimelic acid and azelaic acid in uremic serum were determined using a mass fragmentographic technique. Concentration of succinic acid in uremic serum was comparable to that in normal serum, whereas concentrations of adipic acid, 3-methyladipic acid, 2,4-dimethyladipic acid, pimelic acid and azelaic acid were highly elevated in uremic serum.

Adipates↗
PubMed1979

The excretion of C6-C10-dicarboxylic acids in the urine of newborn infants during starvation. Evidence for omega-oxidation of fatty acids in the newborn.

The excretion of C6-C10-dicarboxylic acids, i.e. adipic, suberic and sebacic acids, was measured during the three first days of life in 3 fasting newborns, 2 newborns fed with isocaloric glucose and 2 newborns given mothers'-milk. On the second and third day of life the starved children excreted 27-84 mmol adipic acid/mol creatinine, 6-22 mmol suberic acid/mol creatinine and 4-7 mmol sebacic acid/mol creatinine. The excretion of C6-C10-dicarboxylic acids in the neonates given glucose or mothers'-milk was, for the first three days of life, 0-9 mmol adipic acid/mol creatinine, 0-10 mmol suberic acid/mol creatinine and 0-4 mmol sebacic acid/mol creatinine. The latter amounts are equivalent to the excretion of dicarboxylic acids in older children. It is argued that the detected dicarboxylic acids are formed by omega-oxidation of long-chain monocarboxylic acids followed by beta-oxidation, and that the excreted amounts reflect omega-oxidation activity. It is speculated that the substantial omega-oxidation activity in the starving newborn serve to provide succinyl-CoA-substrate for the citric acid cycle and for gluconeogenesis.

Adipates↗
PubMed1975

The metabolism of benzoate by Moraxella species through anaerobic nitrate respiration. Evidence for a reductive pathway.

Moraxella sp. isolated from soil grows anaerobically on benzoate by nitrate respiration; nitrate or nitrite are obligatory electron acceptors, being reduced to molecular N2 during the catabolism of the substrate. This bacterium also grows aerobically on benzoate. 2. Aerobically, benzoate is metabolized by ortho cleavage of catechol followed by the beta-oxoadipate pathway. 3. Cells of Moraxella grown anaerobically on benzoate are devoid of ortho and meta cleavage enzymes; cyclohexanecarboxylate and 2-hydroxycyclohexanecarboxylate were detected in the anaerobic culture fluid. 4. [ring-U-14C]Benzoate, incubated anaerobically with cells in nitrate-phosphate buffer, gave rise to labelled 2-hydroxycyclohexanecarboxylate and adipate. When [carboxy-14C]benzoate was used, 2-hydroxycyclohexanecarboxylate was radioactive but the adipate was not labelled. A decarboxylation reaction intervenes at some stage between these two metabolites. 5. The anaerobic metabolism of benzoate by Moraxella sp. through nitrate respiration takes place by the reductive pathway (Dutton & Evans, 1969). Hydrogenation of the aromatic ring probably occurs via cyclohexa-2,5-dienecarboxylate and cyclohex-1-enecarboxylate to give cyclohexanecarboxylate. The biochemistry of this reductive process remains unclear. 6. CoA thiol esterification of cyclohexanecarboxylate followed by beta-oxidation via the unsaturated and hydroxy esters, would afford 2-oxocyclohexanecarboxylate. Subsequent events in the Moraxella culture differ from those occurring with Rhodopseudomonas palustris; decarboxylation precedes hydrolytic cleavage of the alicyclic ring to produce adipate in the former, whereas in the latter the keto ester undergoes direct hydrolytic fission to pimelate.

Anaerobiosis↗
PubMed1975

The metabolism of cyclohexanol by Acinetobacter NCIB 9871.

Acinetobacter NCIB 9871 was isolated by elective culture on cyclohexanol and grows with this compound as sole source of carbon. It displays a restricted growth spectrum, being unable to grow on a wide range of alternative alicyclic alcohols and ketones. Cyclohexanol-grown cells oxidize the growth substrate at a rate of 230 mul of O2/h per mg dry wt with the consumption of 5.65 mumol of O2/mumol substrate. Cyclohexanone is oxidized at a similar rate with the consumption of 4.85 mumol of O2/mumol. 1-Oxa-2-oxocycloheptane and 6-hydroxyhexanoate are both oxidized at the same slow rate of 44 mul of O2/h per mg dry wt and adipate is not oxidized. Studies with cell extracts reveal the presence of inducible dehydrogenases for cyclohexanol, 6-hydroxyhexanoate and 6-oxohexanoate and a monooxygenase, that in conjunction with a lactonase converts cyclohexanone to 6-hydroxyhexanoate. The monooxygenase is therefore presumed to be of the lactone-forming type and the pathway for conversion of cyclohexanol to adipate; cyclohexanol leads to cyclohexanone leads to 1-oxa-2-oxocycloheptane leads to 6-hydroxyhexanoate leads to 6-oxohexanoate leads to adipate; for which key intermediates have been identified chromatographically, is identical with the route for the oxidation of cyclohexanol by Nocardia globerula CL1.

Acinetobacter↗
PubMed1976

Suberylglycine excretion in the urine from a patient with dicarboxylic aciduria.

Suberylglycine (HOOC(CH2)6CONHCH2COOH) was found in the urine from a patient with C6-C10-omega-dicarboxylic aciduria and unexplained episodes of lethargy and unconsciousness. The total excretion of adipic, suberic and sebacic acid ranged from 0.77 to 1.3 mg/mg creatinine after episodes of acute attack of the disease. Suberylglycine, identified by gas chromatography/mass spectrometry, was repeatedly found in the urine samples. The amount of this conjugate ranged from 0.2 to 0.5 mg/mg creatinine. The precursors of the dicarboxylic acids are suggested to be long chain monocarboxylic acids, oxidized through omega- and beta-oxidation to adipic, suberic and sebacic acid. Suberylglycine is subsequently formed by glycine-N-acylase catalyzed conjugation.

Adipates↗