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Urine adipic acid

A half-life of 6 min for metabolism of di(2-ethylhexyl) adipate has been determined in rat small intestinal mucous membrane homogenates. The dominant urinary metabolite of di(2-ethylhexyl) adipate (500 mg/kg bw) in male Wistar rats is adipic acid, which accoimts for 20-30% of the administered oral dose. The other major metabolite which was found only in the stomach is mono(2-ethylhexyl) adipate (Takahashi et al., 1981). In cynomolgus monkeys, the glucuronide of mono(2-ethyl-hexyl) adipate and traces of unchanged di(2-ethylhexyl) adipate were foimd in the urine (BUA, 1996). [Pg.157]

Table 2.1.8 The primary defects of amino acid metabolism and the corresponding changes of plasma or urine amino acid levels. AA amino acid, AAA a-amino-adipic acid,... Table 2.1.8 The primary defects of amino acid metabolism and the corresponding changes of plasma or urine amino acid levels. AA amino acid, AAA a-amino-adipic acid,...
The urinary elimination of glutaric acid increases in rats after administration of L-lysine (T15), a fact which is in accordance with the known metabolic route leading from lysine to glutaric acid via pipecolic acid (R8) (Fig. 5). Another intermediate of that metabolic sequence, a-keto-adipic acid, is foimd in urine after administration of lysine to the rat, the amount representing about 2 % of that of the administered L-lysine... [Pg.72]

Adipic Acid. Adipic acid was first shown in normal urine during paper chromatographic studies (N13) the daily normal elimination lies between 1.3 and 2.5 mg (T18) but increases after administration of e-aminocaproic acid, a part of which would be transformed into adipic acid by oxidative deamination (T18). After administration of adipic acid, one finds a larger amount in the urine than when administering glutaric acid (W8). [Pg.73]

Lofata Burne was excreting dicarboxylic acids in her urine, particularly adipic acid (which has 6 carbons) and suberic acid (which has 8 carbons). [Pg.431]

The name oxalic acid is derived from one of its sources in the biological world, namely, plants of the genus Oxalis, one of which is rhubarb. Oxalic acid also occurs in human and animal urine, and calcium oxalate (the calcium salt of oxalic acid) is a major component of kidney stones. Adipic acid is one of the two monomers required for the synthesis of the polymer nylon 66. The U.S. chemical industry produces approximately 1.8 billion pounds of adipic acid annually, solely for the synthesis of nylon 66 (Section 16.4A). [Pg.459]

A sixth case, occurring in a 15-year-old boy, was reported by Halvorsen etal. (1979). Their patient, who was the second son of unrelated parents, had a history of coma and/or acidosis with ketonuria between 1 and 4 years of age, developing later in childhood episodes headaches, but with normal physical and mental development to 15 years of age. Large quantitities of 3-hydroxy-butyrate, 2-methyl-3-hydroxybutyrate and tiglylglycine were found in his urine together with increased amounts of adipic acid. No methylacetoacetate or acetoacetate were observed. A probable partial deficiency of )8-ketothiolase was postulated. [Pg.285]

Tanaka, K. (1972), On the mode of action of hypoglycin A. III. Isolation and identification of c/5-4-decene-l,10-dioic, cis cw-4,7-decadiene-l,10-dioic, cis-4-octene-l,8-dioic, glutaric and adipic acids, N-(methylenecyclopropyl)acetylglycine and V-isovalerylglycine from urine of hypoglycin A-treated rats. /. Biol. Chem.y 247, 7465. [Pg.381]

In six male volunteers given 46 mg deuterium-labelled di(2-ethylhexyl) adipate [approx. 0.5 mg/kg bw] in com oil, 2-ethylhexanoic acid was the only metabolite that could be determined in the plasma. It had an elimination half-life of 1.65 h. In urine, the following metabolites were identified (percentage fraction of administered deuterium label) 2-ethylhexanoic acid (8.6%), 2-ethyl-5-hydroxyhexanoic acid (2.6%), 2-ethyl-1,6-hexanedioic acid (0.7%), 2-ethyl-5-ketohexanoic acid (0.2%) and 2-ethylhexanol (0.1%). The half-life for elimination of all metabolites excreted in the urine averaged 1.5 h, and none of the metabolites could be detected after 36 h (Loftus et al, 1993). [Pg.157]

One of the most frequent defects of fatty acid oxidation is deficiency of a mitochondrial acyl-CoA dehydrogenase.50 If the long-chain-specific enzyme is lacking, the rate of P oxidation of such substrates as octanoate is much less than normal and afflicted individuals excrete in their urine hexanedioic (adipic), octanedioic, and decanedioic acids, all products of co oxidation.54 Much more common is the lack of the mitochondrial medium-chain acyl-CoA dehydrogenase. Again, dicarboxylic acids, which are presumably generated by 0) oxidation in the peroxisomes, are present in blood and urine. Patients must avoid fasting and may benefit from extra carnitine. [Pg.945]

In known metabolic states and disorders, the nature of metabolites excreted at abnormal levels has been identified by GC-MS. Examples of this are adipic and suberic acids found in urine from ketotic patients [347], 2-hydroxybutyric acid from patients with lactic acidosis [348], and methylcitric acid (2-hydroxybutan-l,2,3-tricarboxylic acid) [349] in a case of propionic acidemia [350,351]. In the latter instance, the methylcitric acid is thought to be due to the condensation of accumulated propionyl CoA with oxaloacetate [349]. Increased amounts of odd-numbered fatty acids present in the tissues of these patients due to the involvement of the propionyl CoA in fatty acid synthesis, have also been characterised [278]. A deficiency in a-methylacetoacetyl CoA thiolase enzyme in the isoleucine pathway prevents the conversion of a-methylacetoacetyl CoA to propionyl CoA and acetyl CoA [352,353]. The resultant urinary excretion of large amounts of 2-hydroxy-3-methylbutanoic acid (a-methyl-/3-hydroxybutyric acid) and an excess of a-methylacetoacetate and often tiglyl glycine are readily detected and identified by GC-MS. [Pg.64]

Witten et al. (1973) identified adipic and 3-methyladipic acids and also reported the presence in urine, using GC-MS, of aconitic and isocitric acids in addition to citrate. Mamer et al, (1971) reported the occurrence of several hydroxyaliphatic acids in addition to those already identified by other workers, and Mamer and Tjoa have identified 2-ethylhydracrylic acid in urine derived from isoleucine metabolism (Mamer and Tjoa, 1974). Urine from healthy children and adults may contain low amounts of aliphatic dicarboxylic acids of chain length C4-C8 (Lawson et ai, 1976). Pettersen and Stokke (1973) reported a series of 3-methyl-branched C4-C8 dicarboxylic acids in urine from normal subjects, and Lindstedt and co-workers have identified other dicarboxylic acids with cyclopropane rings and acetylenic bonds as well as a series of cis and trans mono-unsaturated aliphatic dicarboxylic acids (Lindstedt et al., 1974,1976 Lindstedt and Steen, 1975). [Pg.166]

Fig. 10.19 Chromatogram of organic acids extracted using ethyl acetate from the urine of a patient with 3-hydroxy-3-methylglutaric aciduria and separated as their trimethylsilyl derivatives on 5 per cent SE 52 on Chromosorb W (AW-DMCS, 100-120 mesh) using temperature programming from 75°C to 220°C at 2°C min with initial and final isothermal delays of 10 min. Peak identifications are 1, 3-hydroxyisovalerate 2, hydroxycaproate isomer 3, glutarate 4, 3-methylglutarate 5 and 6, 3-methyl-glutaconate peaks 7, adipate 8, 4-phenylbutyrate (internal standard) 9, 3-hydroxy-3-methylglutarate 10, ascorbate. (Redrawn with modifications from Duran ct. a/., 1978)... Fig. 10.19 Chromatogram of organic acids extracted using ethyl acetate from the urine of a patient with 3-hydroxy-3-methylglutaric aciduria and separated as their trimethylsilyl derivatives on 5 per cent SE 52 on Chromosorb W (AW-DMCS, 100-120 mesh) using temperature programming from 75°C to 220°C at 2°C min with initial and final isothermal delays of 10 min. Peak identifications are 1, 3-hydroxyisovalerate 2, hydroxycaproate isomer 3, glutarate 4, 3-methylglutarate 5 and 6, 3-methyl-glutaconate peaks 7, adipate 8, 4-phenylbutyrate (internal standard) 9, 3-hydroxy-3-methylglutarate 10, ascorbate. (Redrawn with modifications from Duran ct. a/., 1978)...
Fig. 11.2 Total ion current chromatogram (Varian MAT 44 GC-MS) of organic acids extracted using ethyl acetate and diethyl ether from the urine of a patient with propionic acidaemia and separated as their trimethylsilyl derivatives on a 25 m SE-54 WCOT capillary column using temperature programming from 70°C to 220°C at 4 C min Peak identifications are 1, lactate 2, 3-hydroxypropionate 3, 3-hydroxybutyrate 4, 2-methyl-3-hydroxybutyrate 5, 3-hydroxyisovalerate 6, 3-hydroxy- -valerate 7, aceto-acetate 8 and 9, 2-methyl-3-hydroxyvalerate 10, 3-oxovalerate 11, 2-methyl-3-oxo-valerate (isomer 1) 12,2-methylacetoacetate 13,2-methyl-3-oxovalerate (isomer 2) 14 propionylglycine 15, glutarate 16, adipate 17, 5-hydroxymethyl-2-furoate 18, 2-hydroxyglutarate 19,3-hydroxy-3-methylglutarate 20,4-hydroxyphenylacetate 21 and 22, methylcitrate 23,4-hydroxyphenyl-lactate 24, palmitate. (Redrawn with modifications from Truscott et al., 1979)... Fig. 11.2 Total ion current chromatogram (Varian MAT 44 GC-MS) of organic acids extracted using ethyl acetate and diethyl ether from the urine of a patient with propionic acidaemia and separated as their trimethylsilyl derivatives on a 25 m SE-54 WCOT capillary column using temperature programming from 70°C to 220°C at 4 C min Peak identifications are 1, lactate 2, 3-hydroxypropionate 3, 3-hydroxybutyrate 4, 2-methyl-3-hydroxybutyrate 5, 3-hydroxyisovalerate 6, 3-hydroxy- -valerate 7, aceto-acetate 8 and 9, 2-methyl-3-hydroxyvalerate 10, 3-oxovalerate 11, 2-methyl-3-oxo-valerate (isomer 1) 12,2-methylacetoacetate 13,2-methyl-3-oxovalerate (isomer 2) 14 propionylglycine 15, glutarate 16, adipate 17, 5-hydroxymethyl-2-furoate 18, 2-hydroxyglutarate 19,3-hydroxy-3-methylglutarate 20,4-hydroxyphenylacetate 21 and 22, methylcitrate 23,4-hydroxyphenyl-lactate 24, palmitate. (Redrawn with modifications from Truscott et al., 1979)...
This chapter describes the case reports of these enzyme deficiencies and the underlying biochemistry of the disorders and their associations. It is not the intention to discuss keto acidosis associated with other diseases, for example juvenile diabetes, or ketogenesis and its control which are reviewed elsewhere (Wildenhoff, 1975, 1977 McGarry and Foster, 1976 Halperin, 1977). In addition to the common occurrence of 3-hydroxybutyrate and acetoacetate in body fluids of patients with keto acidosis, secondary organic acids have been observed in urine, including adipic and suberic acids (Pettersen et aL, 1972), 3-hydroxyisovaleric acid (Landaas, 1974), 3-hydroxyisobutyric acid and 2-methyl-3-hydroxybutyric acid (Landaas, 1975). The dicarboxylic acids occur as a result of initial co-oxidation of accumulating long-chain fatty acids followed by )8-oxidation (Pettersen, 1972), and metabolites of the branched-chain amino acids occur because of inhibition of their metabolic pathways by 3-hydroxybutyrate and acetoacetate (Landaas and Jakobs, 1977). [Pg.332]

Pettersen, J.E., Jellum, E. and Eldjarn, L. (1972), The occurrence of adipic and suberic acid in urine from ketotic patients. Clin. Chim. Acta, 38,17. [Pg.336]


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