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PubMed1990

Recurrent, familial Reye-like syndrome with a new complex amino and organic aciduria.

Five of 13 siblings from a Jewish-Ashkenazi family suffered from recurrent Reye-like episodes. During attacks, these patients excreted alpha-keto-adipic, alpha-hydroxy-adipic, and alpha-aminoadipic acids, branched-chain keto acids and saccharopine in addition to lactic, pyruvic, and dicarboxylic acids characteristic of Reye syndrome. The serum concentrations of citrulline and alpha-amino-adipic acid were elevated and carnitine was at the upper limit of the normal range. Serum acetoacetate level was 4-5 times the beta-hydroxybutyrate level, but the pyruvate/lactate ratio was normal. Notably, plasma ketone bodies were lower than expected from the degree of catabolism. When the patients were symptom-free, no abnormal amino or organic acids in serum or urine were detected. These findings might be interpreted as a functional impairment at three different biochemical sites: fatty acid beta-oxidation, dehydrogenase complexes of the pyruvic, alpha-ketoglutaric, alpha-ketoadipic, and branched-chain keto acids, and pyruvate carboxylase. We suggest that in this hereditary disorder a toxic substance, exogenously or endogenously derived, interfered at multiple sites in different metabolic pathways.

Adipates↗
PubMed1976

Metabolism of alpha-aminoadipic and alpha-ketoadipic acids: studies using rat and beef liver, and human leukocytes.

The reported studies have shown that alpha-DL-amino [1-14C]adipic acid is metabolized to radioactive alpha-ketoadipic acid and then to 14CO2 in rat and beef liver homogenates. It was also demonstrated that alpha-keto [1-14C]adipic acid is decarboxylated to 14CO2. The effects of several co-factors and other variables, i.e. alpha-ketoglutarate, pyridoxal phosphate, NAD, thiamine pyrophosphate (TPP), FAD, LA, and pH have also been delimited. These reactions and the effects of the co-factors were also established in freshly drawn leukocytes. Using the methods outlined, a technique for studying the metabolism of alpha-amino-adipate and alpha-ketoadipate in the leukocytes from 10 ml of blood was developed.

2-Aminoadipic Acid↗
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↗
PubMed1980

Non-ketotic C6-C10-dicarboxylic aciduria: biochemical investigations of two cases.

Two boys, who are not related, with hypoglycemia and C6-C10-dicarboxylic aciduria were investigated. Besides substantial amounts of adipic, suberic and sebacic acids, the urinary metabolic profile of organic acids contained 5-OH-caproic acid and caproylglycine. During acute attacks the concentrations of adipic, suberic and sebacic acids were 300--530, 160--200 and 35--200 micrograms/mg creatinine, respectively, and the excretions of 5-OH-caproic acid and caproylglycine were 75--330 and 41--260 micrograms/mg creatinine, respectively. It is argued that the biosynthesis of adipic acid passes through an omega-oxidation, that the production of 5-OH-caproic acid is caused by an omega-1-oxidation, and that caproylglycine formation passes through a glycine-N-acylase catalysed conjugation of accumulated caproic acid in the patients. Suberic acid and sebacic acid are in the same way omega-oxidation products of accumulated caprylic acid and capric acid, respectively. From the excretion pattern presented it is hypothesized that the patients suffer from a defect in the dehydrogenation of fatty acids in the beta-oxidation pathway. The biological significance of the findings is discussed.

Adipates↗
PubMed1989

Urinary 3-hydroxyadipic acid 3,6-lactone: structural identification and effect of fasting in adults and children.

Increased urinary excretion of medium-chain dicarboxylic acids is a general feature of disordered fatty acid metabolism. The physiological role of the metabolic pathways involved in dicarboxylic acid production has been a subject of controversy. In the present investigation, the existence of 3-hydroxyadipic acid 3,6-lactone, possibly representing a metabolic intermediate in the beta-oxidation of adipic acid to succinic acid, has been demonstrated. The identity of this compound was established by electron-impact mass spectrometry of its trimethylsilyl derivative and by comparison with synthetic authentic samples. 3-Hydroxyadipic acid 3,6-lactone is present in almost every urine sample we have examined. In the nonfasting state, urinary concentrations of 0.9 +/- 0.5 micrograms/mg creatinine were observed in the adults. During fasting, the urinary excretion of this compound increased with time. It reached 19.1 +/- 8.5 micrograms/mg creatinine by the end of the third day. The responses in children were even higher; urinary concentrations of 82 +/- 50 micrograms/mg creatinine were observed by the end of 36 hours. The urinary excretion of the lactone is closely correlated (r2 = 0.8) with that of adipic acid, an indicator of fatty acid omega-oxidation activity. Non-ketotic dicarboxylic aciduria appears to vary in different defects based on the ratio of urinary lactone to adipic acid.

Adipates↗
PubMed2006

Interaction of metabolites with R. rhodochrous during the biodegradation of di-ester plasticizers.

The commonly used plasticizers di-ethylhexyl phthalate (DEHP) and di-ethylhexyl adipate (DEHA) are known to partially degrade in the presence of soil microorganisms, such as Rhodococcus rhodochrous, releasing persistent and toxic metabolites. The metabolites adipic acid and 2-ethylhexanol were both shown to inhibit growth of the degrading microbe. 2-Ethylhexanol enhanced the activity of ethanol dehydrogenase - an enzyme involved in its metabolism - but the activity of this enzyme was inhibited by adipic acid. The metabolite usually seen in the highest concentrations - 2-ethylhexanoic acid - did not exhibit any evidence of inhibition. It was shown that the high concentration of this metabolite was due to the inability of R. rhodochrous to degrade it. Comparisons with other small carboxylic acids supported the argument that the ethyl branch was the reason for the resistance of 2-ethylhexanoic acid to degradation. The hydrophobicity of the cell surface was shown to be a factor in plasticizer degradation. The primary carbon source could be either water-soluble or hydrophobic and a hydrophobic substrate led to a cell surface that attracted the plasticizer and facilitated degradation. The most hydrophobic of the plasticizers, DEHP, was particularly sensitive to this effect.

Adipates↗
PubMed2004

Chemoenzymatic synthesis of optically active, biodegradable polymers based on phenyl- and naphthyl-ethanols esterified with divinyladipate.

For the purpose of developing a new synthetic polymer containing an asymmetric molecule branch, three racemic alcohols, i.e. 1-phenylethanol, 1-(4-methylphenyl)ethanol and 1-(2-naphthyl)ethanol, were esterified enzymatically with divinyladipate using a lipase from Pseudomonas cepacia. The enzymatic acylation of alcohols produced monoacylated products. Optically active polymerizable monomers, (R)-vinyl adipic acid (phenyl-1-yl) ethyl ester, (R)-vinyl adipic acid (4-methylphenyl-1-yl) ethyl ester and (R)-vinyl adipic acid (2-naphthyl-1-yl) ethyl ester with enantiometric excesses over 99%, 96% and 99%, respectively, were obtained. Each optically active monomer was then subjected to free radical polymerization, to give polymers having a number average molecular weight of 2.9 x 10(3) - 2.2 x 10(4). These polymers are considered useful as optically active polymers having biodegradability.

Adipates↗
PubMedDate not supplied

Migration from plasticized films into foods. 6. Hydrolysis of polymeric plasticizers under simulated gastric and intestinal conditions.

The polymeric plasticizers poly(butylene adipate) and poly(propylene adipate), and a low molecular weight oligomer fraction from each, were exposed in vitro to simulated gastric and intestinal hydrolysis in order to study their likely fate after ingestion of foods contaminated by migration from plastics packaging. Analysis for loss of the parent compounds indicated that partial hydrolysis occurred under simulated gastric conditions, with the low molecular weight oligomers being the most susceptible. Analysis for one of the starting materials, adipic acid, revealed however that the hydrolysis did not result in a significant conversion to free monomer under either simulated gastric or intestinal conditions. This is explained on the basis of partial hydrolysis of the plasticizers to smaller oligomer units but with the more resistant ester linkages resisting complete breakdown to monomer.

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↗
PubMed2001

Cloning and genetic characterization of dca genes required for beta-oxidation of straight-chain dicarboxylic acids in Acinetobacter sp. strain ADP1.

A previous study of deletions in the protocatechuate (pca) region of the Acinetobacter sp. strain ADP1 chromosome revealed that genes required for utilization of the six-carbon dicarboxylic acid, adipic acid, are linked to the pca structural genes. To investigate the genes involved in adipate catabolism, a 33.8-kb SacI fragment, which corrects a deletion spanning this region, was cloned. In addition to containing known pca, qui, and pob genes (for protocatechuate, quinate, and 4-hydroxybenzoate dissimilation), clone pZR8000 contained 10 kb of DNA which was the subject of this investigation. A mutant strain of Escherichia coli DH5alpha, strain EDP1, was isolated that was able to utilize protocatechuate and 4-hydroxybenzoate as growth substrates when EDP1 cells contained pZR8000. Sequence analysis of the new region of DNA on pZR8000 revealed open reading frames predicted to be involved in beta-oxidation. Knockouts of three genes implicated in beta-oxidation steps were introduced into the chromosome of Acinetobacter sp. strain ADP1. Each of the mutants was unable to grow with adipate. Because the mutants were affected in their ability to utilize additional saturated, straight-chain dicarboxylic acids, the newly discovered 10 kb of DNA was termed the dca (dicarboxylic acid) region. Mutant strains included one with a deletion in dcaA (encoding an acyl coenzyme A [acyl-CoA] dehydrogenase homolog), one with a deletion in dcaE (encoding an enoyl-CoA hydratase homolog), and one with a deletion in dcaH (encoding a hydroxyacyl-CoA dehydrogenase homolog). Data on the dca region should help us probe the functional significance and interrelationships of clustered genetic elements in this section of the Acinetobacter chromosome.

Acinetobacter↗
PubMed1988

In situ metabolism of 1,omega medium chain dicarboxylic acids in the liver of intact rats as detected by 13C and 1H NMR.

The hepatic metabolism of 1,omega-dodecanedioic acid, a physiologically relevant representative of the medium-chain dicarboxylic acid family, has been studied by a combination of in vivo and in vitro 13C and 1H NMR spectroscopic techniques. Rats in different nutritional or hormonal situations were infused with [1,12-13C2]- or [1,2,11,12-13C4]dodecanedioic acid, and the kinetics of 13C label appearance as well as the final relative concentrations of metabolic products were measured noninvasively in the liver of the intact rat by 13C NMR spectroscopy. Perchloric acid and chloroform/methanol extracts of liver biopsies obtained at the end of the infusion period were further analyzed by high resolution 13C NMR and one-dimensional and two-dimensional COSY and J-resolved 1H NMR. [1-13C]- and [1,2-13C2]adipic acids were the main end products of the in vivo metabolism of [1,12-13C2]- or [1,2,11,12-13C4]dodecanedioic acids, respectively, indicating that the beta-oxidation pathway of medium-chain dicarboxylic acids proceeds in situ monodirectionally. [1-13C]Adipic acid, the main product of peroxisomal beta-oxidation, could also be detected in situ. This finding, together with the in vivo and in vitro absence of signals characteristic of intramitochondrial oxidation of [1-13C]acetyl-coenzyme A, provide a strong evidence supporting a predominant contribution of the peroxisomal beta-oxidation system to the overall oxidation of these compounds in vivo. Homonuclear two-dimensional COSY 1H NMR spectra of acid extracts from rat liver provided a convenient method of analyzing the metabolic repercussions of dicarboxylic acid accumulation, revealing a decrease in the hepatic concentration of beta-hydroxybutyrate and an accumulation of adipic acid and the amino acid L-lysine.

Adipates↗
PubMed2006

Investigation into the erosion mechanism of salicylate-based poly(anhydride-esters).

Salicylate-based poly(anhydride-esters), collectively referred to as PolyAspirin, hydrolytically degrade into salicylic acid, a nonsteroidal anti-inflammatory drug (NSAID). The variations of the poly(anhydride-ester) investigated in this article are linked by adipic acid, suberic acid, or sebacic acid. To elucidate the erosion mechanism of these polymers, water uptake, mass loss, contact angle, and changes in device thickness were monitored as a function of in vitro degradation time. The polymers examined here appeared to primarily undergo surface erosion. The adipate homopolymer absorbed the most water and therefore swelled more than the other versions of the poly(anhydride-ester). Additionally, the adipate homopolymer eroded most quickly. Increasing the length of the linker moiety decreased the driving force for hydrolysis, which prolonged the lifetime of the polymer sample.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Structure investigation of Maltacine C1a, C1b, C2a and C2b-cyclic peptide lactones of the Maltacine complex from Bacillus subtilis.

A new complex of cyclic peptide lactone antibiotics from Bacillus subtilis, which we named Maltacines, has recently been described. The structure elucidation of four of them is reported in this paper. The amino acid sequences and structures of the peptides were found by MS(n) of the ring-opened linear peptides, which gave uninterrupted sequences of Bn and Y''n ions. The identities of three unknown residues in the sequences were solved by a combination of derivatisation with phenylisothiocyanate (PITC), high-resolution mass spectrometry and H/D exchange. The nature and position of the cyclic structure was disclosed by a chemo-selective ring opening with Na18OH and was found to be a lactone formed between a hydroxyl of residue number 4 and the C-terminal amino acid number 12. For verification of the structure of the B2+ ion, peptides with different combinations of P/Q and P/K at the N-terminus were synthesised. The structure of the four peptides were found to be: C1a and C2a: cyclo-4,12(P-Q-Y-Adip-V-E-T-Y-Orn-103-Y-I-OH) and C1b/C2b: cyclo-4,12(P-Q-Y-Adip-V-E-T-Y-K-103-Y-I-OH). Adip = aminodihydroxy pentanoic acid.

Amino Acid Sequence↗
PubMed2005

Mass spectrometric investigation of Maltacines E1a and E1b--two members of the Maltacine family of peptide antibiotics.

We have recently described the discovery of the Maltacines--a new family of cyclic peptide antibiotics from Bacillus subtilis. In this paper the mass spectrometric characterisation of two of the members is reported. A chemoselective ring opening with base to give the linear peptides was necessary before mass spectrometric characterisation could be performed. MS(n) of the singly and doubly charged protonated molecules gave uninterrupted series of Bn and Y''n ions that allowed determination of the amino acid sequence. By using a combination of derivatisation with phenylisothiocyanate (PITC), high-resolution mass spectrometry and H/D exchange, the identities of three unknown residues were determined. The nature and position of the cyclic structure were disclosed by a chemoselective ring opening with Na 18OH and it was found to be a lactone formed between a hydroxyl of residue number 4 and the C-terminal amino acid number 12. Peptides with different combinations of P/Q and P/K at the N-terminus were synthesised to verify the sequence of the N-terminal B2 ion. The structure of the two peptides is proposed to be: E1a: cyclo-4,12(P-Q-Y-Adip-V-E-T-Y-Orn-S-Y-I-OH) and E1b: cyclo-4,12(P-Q-Y-Adip-V-E-T-Y-K-S-Y-I-OH). Adip = (2-amino-4,5-dihydroxypentanoic acid).

Amino Acid Sequence↗
PubMed1990

Urinary organic acid profiles in fatty Zucker rats: indications for impaired oxidation of butyrate and hexanoate.

The urinary excretion of 45 organic acids, monitored by gas-liquid chromatography, was compared in fatty (fa/fa) and lean (Fa/?) Zucker rats maintained on a chemically simplified diet. At the age of 6, 16, and 22 weeks, fatty rats excreted more of the various organic acids than their lean counterparts. However, the greatest difference was in the excretion of ethylmalonate, even when excretion data were normalized to body weight. The next highest excretion difference was in adipate and an unknown compound, and the third highest in pyruvate. A second group of rats examined at 7 weeks also excreted an excess of these four acids, as well as glucuronate and indole-3-acetate. The excessive excretion of ethylmalonate and adipate, which is characteristic of human genetic defects in short- and medium-chain fatty acid oxidation, suggested that the oxidation of butyrate and hexanoate might be impaired in the fatty rat. Thus, as a test of their capacity to oxidize medium- and short-chain fatty acids, two groups of fatty and lean rats were transferred to diets enriched with either trioctanoylglyceride, a medium-chain triglyceride (MCT), or sodium butyrate, a short-chain fatty acid. Both lean and fatty rats on the MCT diet, but only the lean rats on the butyrate-enriched diet, increased their excretion of adipate. However, on both the MCT and butyrate diet, ethylmalonate excretion increased only in lean rats, almost reaching amounts found previously in fatty rats. These results suggest that the fatty rat has an impairment of the beta-oxidation of butyrate and hexanoate, a defect that might increase intracellular concentrations of butyryl-CoA, the optimal primer for the synthesis of long-chain fatty acids.

Acids↗
PubMed1991

Cytotoxicity of dibasic esters (DBE) metabolites in rat nasal explants.

Dibasic esters (DBE) is a solvent mixture of dimethyl adipate, dimethyl glutarate, and dimethyl succinate which causes a selective degeneration of the nasal olfactory epithelium in rats following a 90-day inhalation exposure. In short-term cultures of rat nasal explants, it has been demonstrated that DBE cytotoxicity is due to a carboxylesterase-mediated activation. In the present study, the putative toxic metabolites of DBE, the monomethyl esters and the dicarboxylic acids, were evaluated in the nasal explant system at concentrations ranging from 10 to 50 mM. Monomethyl adipate (MMA), monomethyl glutarate (MMG), and monomethyl succinate (MMS) induced increases in nasal explant acid phosphatase release, a biochemical index of cytotoxicity. The nasal explant-mediated metabolism of MMA and MMG to their corresponding diacids paralleled the increases in acid phosphatase release. A carboxylesterase inhibitor, bis(p-nitrophenyl)phosphate (BNPP), inhibited both the cytotoxicity and the hydrolysis of MMA and MMG in the nasal explant system. The metabolism and cytotoxicity of MMS was not attenuated as effectively by BNPP pretreatment. Adipate, glutarate, and succinate induced concentration-related increases in cytotoxicity in the nasal explant system. These dicarboxylic acids were neither metabolized nor utilized significantly by the nasal explants. Diacid-induced cytotoxicity was not attenuated by BNPP pretreatment. This study further established the utility of the nasal explant system for evaluating cytotoxicity of organic esters in vitro. It was established that both the monomethyl ester and diacid metabolites are cytotoxic in rat nasal explants. Finally, it was concluded that although both the monomethyl esters and the diacids contribute to the cytotoxic potential of DBE in vitro, it is critical to establish if one or both of these are formed in vivo in order to identify the ultimate toxic metabolite of DBE.

Acid Phosphatase↗
PubMed2000

Solvent-free fabrication of micro-porous polyurethane amide and polyurethane-urea scaffolds for repair and replacement of the knee-joint meniscus.

New porous polyurethane urea and polyurethane amide scaffolds for meniscal reconstruction have been developed in a solvent-free process. As soft segments, copolymers of 50/50 L-lactide/epsilon-caprolactone have been used. After terminating the soft segment with diisocyanates, chain extension was performed with adipic acid and water. Reaction between the isocyanate groups and adipic acid or water provides carbon dioxide and results in a porous polymer. Extra hydroxyl-terminated prepolymer was added in order to regulate the amount of carbon dioxide formed in the foaming reaction. Furthermore, salt crystals ranging in size from 150 to 355 microm were added in order to induce macroporosity. The pore size was regulated by addition of surfactant and by the use of ultrasonic waves. The resulting porous polymer scaffolds exhibit good mechanical properties like a high-compression modulus of 150 kPa. Chain extension with adipic acid results in better mechanical properties due to better defined hard segments. This results from the lower nucleophilicity of carboxylic acids compared to water and alcohols. By adjusting the reaction conditions, materials in which macropores are interconnected by micropores can be obtained. On degradation only non-toxic products will be released; importantly, the materials were obtained by a simple, reproducible and solvent-free procedure.

Knee Injuries↗
PubMedDate not supplied

Lipase-catalyzed polycondensations: effect of substrates and solvent on chain formation, dispersity, and end-group structure.

The effects of substrates and solvent on polymer formation, number-average molecular weight (M(n)), polydispersity, and end-group structure for lipase-catalyzed polycondensations were investigated. Diphenyl ether was found to be the preferred solvent for the polyesterification of adipic acid and 1,8-octanediol giving a M(n) of 28 500 (48 h, 70 degrees C). The effect of varying the alkylene chain length of diols and diacids on the molecular weight distribution and the polymer end-group structure was assessed. A series of diacids (succinic, glutaric, adipic, and sebacic acid) and diols (1,4-butanediol, 1,6-hexanediol, and 1,8-octanediol) were polymerized in solution and in bulk. It was found that reactions involving monomers having longer alkylene chain lengths of diacids (sebacic and adipic acid) and diols (1,8-octanediol and 1,6-hexanediol) give a higher reactivity than reactions of shorter chain-length diacids (succinic and glutaric acid) and 1,4-butanediol. The bulk lipase-catalyzed condensation reactions were feasible, but the use of diphenyl ether gave higher M(n) values (42,400 g/mol in 3 days at 70 degrees C). The polydispersity varied little over the conditions studied giving values </=2. No specific trend with respect to end-group structure as a function of time was observed. At 70 degrees C, the retention of catalyst activity in the bulk was independent of substrate structure but was higher when reactions were conducted in diphenyl ether than in bulk.

Catalysis↗