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At least 19 recordsLinked to original sources
PubMed1982

Gas-liquid chromatographic determination of adipate content of acetylated di-starch adipate.

A gas-liquid chromatographic method is described for rapid, quantitative determination of adipate content of acetylated di-starch adipate. The adipate group is very labile and, under mild alkaline conditions at ambient temperature, is easily hydrolyzed from the starch. Free adipic acid is formed by acidification of the solution with HCl, and then extracted with ethyl acetate. Ethyl acetate is removed under vacuum distillation, and a silyl derivative of the adipic acid is formed. Glutaric acid internal standard is introduced into the original starch sample before hydrolysis. An aliquot of the silylated solution is injected into a gas chromatograph fitted with a column having silicone oil as the active phase. A flame ionization detector is also incorporated. Results correlate well the amount of adipylating reagent used. No adipic acid is detectable when a hydrolyzed, extracted sample of acetylated di-starch adipate is subjected to a second extraction. Recovery levels of adipic acid, from starches fortified with 100-500 ppm, are in the range of 97-102.5%.

Adipates↗
PubMed1997

Fabrication of microcapsules using poly(ethylene adipate) and a blend of poly(ethylene adipate) with poly(hydroxybutyrate-hydroxyvalerate): incorporation and release of bovine serum albumin.

Spherical reservoir-type microcapsules composed of poly(ethylene adipate) (PEAD) and 20% poly-epsilon-caprolactone (PCL II), poly(hydroxybutyrate-hydroxyvalerate) (P(HB-HV)); 10.8% HV) 20% PCL II and a blend of P(HB-HV)/PEAD 20% PCL II containing bovine serum albumin (BSA; surrogate protein)-loaded agarose have been fabricated using a double emulsion technique with solvent evaporation. P(HB-HV) and PEAD microcapsules had microporous and smooth surfaces, respectively, while blend microcapsules contained a mixture of the two. Irrespective of the fabrication polymer, microcapsules were generated in high yield (> 75%) and BSA incorporation had no significant effect on microcapsule size distribution (8-200 microns). The loss of BSA, both by partitioning into aqueous continuous phase and through the micropores of P(HB-HV) microcapsules as BSA-loaded agarose during the precipitation of the fabrication polymer concomitant with solvent evaporation, resulted in low encapsulation efficiencies (< 15%). In all cases BSA release could be monitored for up to 26 d and the amount and duration of BSA release from P(HB-HV) 20% PCL II microcapsules was influenced as much by micropore number and diameter as by the extent of reservoir loading, while BSA release from smooth PEAD microcapsules was assumed to be the result of an acute increase in membrane porosity.

Biocompatible Materials↗
PubMed1997

Fabrication of microspheres using blends of poly(ethylene adipate) and poly(ethylene adipate)/poly(hydroxybutyrate-hydroxyvalerate) with poly(caprolactone): incorporation and release of bovine serum albumin.

Spherical microspheres composed of polymer blends 80:20 PEAD/PCL II and 40:40:20 PEAD/P(HB-HV)/PCL II containing a range of BSA loadings have been fabricated using a single emulsion technique with solvent evaporation. 80:20 PEAD/PCL II microspheres had smooth surfaces while 40:40:20 PEAD/P(HB-HV)/PCL II microspheres consisted of a mixture of smooth surfaced, microporous and macroporous microsphere fractions. Irrespective of fabrication polymer, microspheres were produced in high yield (> 75%) and BSA incorporation had no significant effect on microsphere size distribution which ranged from 0.6 to 5 microns and from 2.1 to 50 microns for 80:20 PEAD/PCL II and 40:40:20 PEAD/P(HB-HV)/PCL II microspheres, respectively. The loss of BSA by partitioning into the aqueous phase resulted in low encapsulation efficiencies (< 14.5%). BSA release increased significantly with the-oretical percentage loading but the relationship could not be confirmed when the total cumulative release of BSA was expressed as a percentage of the actual total BSA incorporated. Significant BSA release could be detected for up to 26 days.

Animals↗
PubMed2001

Adipic acid increases plasma lysine but does not improve the efficiency of lysine utilization in swine.

Adipic acid, upon catabolism, results in intermediates that bear a structural similarity to lysine degradation products. The objectives of this research were to determine whether adipic acid affects lysine concentrations in plasma and to evaluate whether adipic acid improves the efficiency of lysine utilization in pigs. In Exp. 1, nursery pigs (n = 14) were fed (for a period of 7 d) either a standard nursery diet or the same diet supplemented with 1% adipic acid to assess effects on plasma amino acid concentrations (plasma collected on d 7). In Exp. 2, nursery pigs (n = 56) were fed (for a period of 15 d) either a control diet or the same diet but deficient in either lysine, threonine, or tryptophan with or without supplemental adipic acid to assess the effects of adipic acid on the efficiency of amino acid utilization. The results from Exp. 1 showed that adipic acid increased plasma lysine (by 18%) but not alpha-amino adipic acid, an intermediate in lysine degradation. Experiment 2 demonstrated that adipic acid did not increase the efficiency of utilization of lysine, threonine, or tryptophan. The lack of effects on alpha-amino adipic acid in Exp. 1 and the lack of a positive effect on the efficiency of utilization of lysine, threonine, and tryptophan suggest that adipic acid does not inhibit the mitochondrial uptake of lysine and(or) its degradation in the mitochondrion. It is concluded that feeding adipic acid increases plasma lysine but does not improve the efficiency of lysine utilization.

Adipates↗
PubMed1981

Urinary excretion of C4--C10-dicarboxylic acids and antiketogenic properties of adipic acid in ketogenic-stimulated rats due to diabetes, long-chain and short-chain monocarboxylic acids.

The urinary excretion of C4--C10-dicarboxylic acids (succinic, adipic, suberic and sebacic acids) and the antiketogenicity of adipic acid have been studied in ketogenic-stimulated rats in three biochemically different states: diabetes, fat-feeding (long-chain monocarboxylic acids) and feeding of hexanoic acid (short-chain monocarboxylic acid). In diabetic rats urinary excretions of adipic and suberic acids were elevated before the rise in urinary excretions of 3-hydroxybutyric acid, i.e. before ketosis appeared. In severe diabetic ketosis sebacic acid was below normal values, whereas the excretion of succinic acid was unaltered. Rats, in which ketosis was provoked by hexanoic acid, had preketotic high urinary excretions of adipic and succinic acids. After ketosis the excretions of succinic acid declined again whereas the excretion of adipic acid rose further, together with that of suberic acid. Moreover, when rats which were ketotic due to treatment with long-chain triacylglycerol or hexanoic acid received 500 mg of adipic acid the urinary excretion of succinic acid rose significantly. However, no changes in succinic acid excretion were seen in diabetic ketotic rats treated with the same amount of adipic acid. Exogenously administered adipic acid was strongly antiketogenic towards ketosis caused by long-chain or short-chain monocarboxylic acids, but had no effect on diabetic ketosis.

Acidosis↗
PubMed2001

Dietary adipic acid reduces ammonia emission from swine excreta.

Adipic acid is only partially catabolized when it is fed to animals, and a portion of it is excreted in urine. The excreted portion may lower urinary pH and, as a result, ammonia emission. The present study tested this hypothesis. In Exp. 1, nursery pigs (n = 14) were fed (for a period of 7 d) either a standard nursery diet or the same diet supplemented with 1% adipic acid to assess effects on urinary pH (collected on d 5 or 6) and in vitro ammonia emission from the collected urine samples that were mixed with control feces. In Exp. 2, grower pigs housed 10 each in one of two chambers were fed a control diet or the same diet supplemented with 1% adipic acid. Ventilated air was quantified and analyzed for ammonia using Fourier transform infrared spectroscopy to determine the effects of feeding 1% adipic acid on ammonia emission. The results from Exp. 1 showed that adipic acid strongly reduced urinary pH (from 7.7 to 5.5, P < 0.05). In vitro ammonia emission from these urine samples was significantly reduced at all the time points evaluated (1, 3, 18, and 46 h with reductions of 94, 93, 70, and 39%, respectively, P < 0.05). Experiment 2 showed that adipic acid supplementation reduced ammonia emission by 25% (P < 0.05), which corresponded to the predicted reduction in ammonia emission based on the reduction in manure pH observed. In conclusion, feeding adipic acid lowers urinary pH and reduces ammonia emission. The reduction in ammonia emission, though, does not correspond to the reduction in urinary pH but corresponds to the reduction in fecal pH as a result of mixing the urine and feces, in which feces act as a strong buffer.

Acid-Base Equilibrium↗
PubMed2001

Isolated adipic aciduria.

Adipic acid can appear, in combination with other dicarboxylic acids, in the urine of patients in a number of underlying metabolic diseases. A child with seizures and mental retardation of unknown etiology who was found to have elevated isolated adipic aciduria on investigation for metabolic diseases is reported. A dietary artifact was suspected, and the adipic aciduria resolved after the child was kept on a specific restricted diet for 3 days. This is the third report of isolated adipic aciduria secondary to food. Findings confirm the previous reports of dietary origin of isolated adipic aciduria and should alert clinicians to such artifact before committing patients to unnecessary treatments.

Adipates↗
PubMed1990

Liberation of 14CO2 from [14C]adipic acid and [14C]octanoic acid by adult rats during riboflavin deficiency and its reversal.

The purpose of the present study was to test the hypothesis that the already well-established mitochondrial lesion in fatty acid oxidation in riboflavin-deficient experimental animals, might be accompanied by an alteration in vivo in the kinetics of oxidation of labelled adipic acid. This dicarboxylic acid was chosen for testing as a metabolic probe because a block in its oxidation was already apparent from urine analysis of riboflavin-deficient animals, whereas the oxidation of medium- or long-chain monocarboxylic acids seemed to be little affected by deficiency in vivo. Female adult Norwegian hooded rats fed on purified diets containing either 15 mg riboflavin/kg diet (controls) or about 0.4 mg/kg (riboflavin-deficient) received an intragastric dose of either [1,6-14C]adipic acid or [1-14C]octanoic acid. Expired carbon dioxide was then collected in an alkaline trap over 3 h, for determination of radioactivity. This test was repeated at intervals for up to 2 weeks following riboflavin repletion of the deficient animals, and in riboflavin-dosed controls. Whereas the rate and extent of [14C]octanoic acid oxidation was not significantly affected by the deficiency or repletion, the extent of [14C]adipic acid oxidation was markedly and significantly increased during repletion of the deficient animals. The time-course indicated a temporary overshoot, followed by a slow return to the control values over 1-2 weeks. Adipate oxidation was also much less affected by a preceding period of overnight starvation, than was octanoate oxidation. Thus, adipic acid (or a related metabolic probe) may have appropriate properties for the design of a functional test of fatty acid oxidation efficiency, during riboflavin deficiency or allied metabolic conditions in human subjects.

Adipates↗
PubMed1989

Metabolism of [14C]adipic acid in riboflavin-deficient rats: a test in vivo for fatty acid oxidation.

Mitochondrial preparations from riboflavin-deficient rats are known to exhibit reduced capacity for the oxidation of fatty acids. During a search for a suitable fatty acid probe for the in vivo exploration of this phenomenon, it became apparent that a dicarboxylic acid, adipic acid, was more promising than a monocarboxylic acid such as octanoic acid. Rats made riboflavin deficient, and controls at various stages of development, were dosed intragastrically with [1,6-14C]adipic acid, and 14CO2 production was measured for 3 h. All animals were then given flavin mononucleotide intragastrically to replete their tissues, and the [14C]adipic acid test was repeated at intervals thereafter. In all groups, repletion produced a highly significant increase in the whole-body adipic acid oxidation index, and reversed the low rates of oxidation which had been observed in nonrepleted, deficient animals. This approach may therefore permit the development of a new functional test for fatty acid oxidation in human riboflavin deficiency, and for other conditions in which fatty acid oxidation pathways are impaired, by the use of nonradioactive [13C]adipic acid.

Adipates↗
PubMed1976

Activated sludge degradation of adipic acid esters.

The biodegradability of three aliphatic adipic acid diesters and a 1,3-butylene glycol adipic acid polyester was determined in acclimated, activated sludge systems. Rapid primary biodegradation from 67 to 99+% was observed at 3- and 13-mg/liter feed levels for di-n-hexyl adipate, di(2-ethylhexyl) adipate, and di(heptyl, nonyl) adipate in 24 h. When acclimated, activated sludge microorganisms were employed as the seed for two carbon dioxide evolution procedures, greater than 75% of the theoretical carbon dioxide was evolved for the three diesters and the polyester in a 35-day test period. The essentially complete biodegradation observed in these studies suggests that these esters would not persist when exposed to similar mixed microbial populations in the environment.

Adipates↗
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↗
PubMed1987

Effect of parbendazole and piperazine adipate on the activity of some enzymes of Ascaridia galli and Heterakis gallinae.

Adult Ascaridia galli and Heterakis gallinae obtained from the fowl (Gallus gallus) were treated in vitro with 10(-2) to 10(-5) M parbendazole and piperazine adipate for 10-60 min at 38 degrees C. Both the compounds at 10(-2) M caused mortality of A. galli and H. gallinae after a maximum of 30 min exposure. The effect of the drugs on the homogenates of the treated worm was investigated. Parbendazole (10(-2) M) inhibited malate oxidation by 68% in A. galli and 62% in H. gallinae. Piperazine adipate (10(-2) M) inhibited malate oxidation by 78% in both parasites. In A. galli oxaloacetate reduction was inhibited by 41 and 26% by 10(-2) M parbendazole and piperazine adipate, respectively; with H. gallinae this inhibition was found to be 39 and 55%, respectively. Aldolase activity in both the parasites was also inhibited by 10(-2) M parbendazole and piperazine adipate. Both compounds caused an inhibition of acid phosphomonoesterase activity, but the activities of lactate dehydrogenase and alkaline phosphomonoesterase were not affected significantly. Parbendazole (10(-2) M) had no significant effect on the cholinesterase activity of these parasites, but piperazine adipate (10(-2) M) caused an inhibition of 96% in A. galli and 93% in H. gallinae. The possible mode of action of the drugs is discussed.

Acid Phosphatase↗
PubMed1991

Non-mutagenicity of 4 metabolites of di(2-ethylhexyl)phthalate (DEHP) and 3 structurally related derivatives of di(2-ethylhexyl)adipate (DEHA) in the Salmonella mutagenicity assay.

Four metabolites of the rat liver carcinogen di(2-ethylhexyl)phthalate (DEHP) (mono-(2-ethylhexyl)phthalate, mono-(2-ethyl-5-hydroxyhexyl)phthalate, mono-(2-ethyl-5-oxohexyl)phthalate, and mono-(5-carboxy-2-ethylpentyl)phthalate) and 3 structurally related derivatives of di(2-ethylhexyl)adipate (DEHA) (mono-(2-ethylhexyl)adipate, mono-(2-ethyl-5-hydroxyhexyl)adipate, and mono-(2-ethyl-5-oxohexyl)adipate) were tested for mutagenicity in the Ames assay using Salmonella typhimurium strains TA97, TA98, TA100, and TA102, with and without a metabolic activation preparation. Aroclor 1254-induced rat liver S9 and DEHP-induced rat liver S9 were used. Concentrations of these compounds up to 1000 micrograms/plate were negative with all tester strains in the presence or absence of metabolic activation.

Adipates↗
PubMed1991

Structure of the adipate complex [Na2(C6H9O4)2(C6H10O4)].2H2O from neutron diffraction at 220 and 295 K.

The crystal structure of sodium hydrogen adipate-adipic acid (2/1) dihydrate, [Na2(C6H9O4)2(C6H10O4)].2H2O, Mr = 518.4, has been determined from neutron diffraction data collected at 220 and 295 K. Crystals are monoclinic, space group C2/m, with Z = 2. At 295 K, a = 9.378 (2), b = 13.379 (5), c = 10.247 (3) A, beta = 95.93 (3) degrees, V = 1278.8 (7) A3, Dn = 1.346, Dm = 1.348 (1) g cm-3 (in dibromomethane/bromobutane), lambda = 1.1588 (2) A, mu = 2.186 cm-1, F(000) = 176.4 fm, R(F2) = 0.108 for all 1995 nonequivalent reflections with sin theta/lambda less than 0.71 A-1. The crystal structure is similar at 220 K except for reduced nuclear mean-square displacements. Hydrogen adipate subunits (called A) are linked end-to-end in infinite chains by very short O...O (2.44 A) hydrogen bonds where the H nuclei are on centers of symmetry within the experimental error. The Na cation is octahedrally coordinated by O atoms from molecules A and also by non-ionized adipic acid molecules (called B). The B molecules have large mean-square nuclear displacements which are described in terms of anharmonicity and disorder.

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↗
PubMed1986

An evaluation of the genotoxic potential of di-isononyl adipate.

Di-isononyl adipate (DINA) is one of a group of adipates used primarily as plasticizers. Concern over the mutagenic and carcinogenic potential of these materials was stimulated by the finding that one member of this class, di-(2-ethylhexyl) adipate (DEHA), induced liver tumors in female mice in a chronic feeding study. Accordingly, the genotoxic potential of DINA was evaluated in a battery of in vitro tests including the Salmonella/mammalian microsome mutagenicity assay, the mouse lymphoma TK +/-assay, and two tests of morphologic transforming ability, the BALB 3T3 and the Syrian hamster embryo in vitro transformation assays. DINA did not exhibit any evidence of mutagenic or transforming potential in any of the assays utilized.

Adipates↗
PubMed1981

Elimination, distribution and metabolism of di-(2-ethylhexyl)adipate (DEHA) in rats.

The excretion, retention, distribution and metabolism of di-(2-ethylhexyl)adipate (DEHA) have been studied in the rat. After oral administration of [14C]DEHA, almost all the dose was excreted within 48 h, predominantly in the urine and as respiratory carbon dioxide. The faecal excretion was low. There was no evidence of the accumulation of radioactivity in any organs or tissues. Adipic acid (AA) was found to be the main urinary metabolite; it was also detected in the digestive tract, blood and liver. In vitro, DEHA was hydrolyzed at a significant rate by tissue preparations prepared from liver, pancreas and small intestine of the rat. These results suggest that orally administered DEHA is rapidly hydrolyzed in the body to form AA without any accumulation of mono-(2-ethylhexyl)adipate (MEHA).

Adipates↗