Hippuric acid and 3-car☐y-4-methyl-5-propyl-2-furanpropionic acid in serum and urine

Liebich, H.M.; Bubeck, J.I.; Pickert, A.; Wahl, G.; Scheiter, A.

doi:10.1016/s0021-9673(00)96096-5

Cited by 24 publications

(7 citation statements)

References 22 publications

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“…Additionally, hippuric acid is a component of non-protein nitrogen containing metabolites which result from protein and nucleic acid metabolism, and are found in urine [ 26 ]. Accordingly, down-regulation of hippuric acid levels has been reported in cases of renal disease [ 27 , 28 ]. In the present study, urinary levels of hippuric acid were significantly decreased in the FA inhalation group.…”

Section: Resultsmentioning

confidence: 99%

Small Molecule Metabolite Biomarker Candidates in Urine from Mice Exposed to Formaldehyde

Zhang

Sun

Chen

et al. 2014

IJMS

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Formaldehyde (FA) is a ubiquitous compound used in a wide variety of industries, and is also a major indoor pollutant emitted from building materials, furniture, etc. Because FA is rapidly metabolized and endogenous to many materials, specific biomarkers for exposure have not been identified. In this study, we identified small metabolite biomarkers in urine that might be related FA exposure. Mice were allowed to inhale FA (0, 4, 8 mg/m3) 6 h per day for 7 consecutive days, and urine samples were collected on the 7th day of exposure. Liquid chromatography coupled with time of flight-mass spectrometry and principal component analysis (PCA) was applied to determine alterations of endogenous metabolites in urine. Additionally, immune toxicity studies were conducted to ensure that any resultant toxic effects could be attributed to inhalation of FA. The results showed a significant decrease in the relative rates of T lymphocyte production in the spleen and thymus of mice exposed to FA. Additionally, decreased superoxide dismutase activity and increased reactive oxygen species levels were found in the isolated spleen cells of exposed mice. A total of 12 small molecules were found to be altered in the urine, and PCA analysis showed that urine from the control and FA exposed groups could be distinguished from each other based on the altered molecules. Hippuric acid and cinnamoylglycine were identified in urine using exact mass and fragment ions. Our results suggest that the pattern of metabolites found in urine is significantly changed following FA inhalation, and hippuric acid and cinnamoylglycine might represent potential biomarker candidates for FA exposure.

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Section: Resultsmentioning

confidence: 99%

Small Molecule Metabolite Biomarker Candidates in Urine from Mice Exposed to Formaldehyde

Zhang

Sun

Chen

et al. 2014

IJMS

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“…Removal of 9 by conventional hemodialysis is difficult owing to its strong binding to plasma protein (78)(79)(80). This property also interferes with the binding of drugs to albumin (81,82). The competitive binding of 9 alters the excretion of various drugs, drug conjugates, and other organic acids (83).…”

Section: Catabolism Of F-acidsmentioning

confidence: 99%

“…Efforts to reduce 9 in serum by continuous ambulatory peritoneal analysis were partly successful (86). Several procedures were elaborated to determine 9 by HPLC methods (82,(90)(91)(92) or by immunoassay (93). By applying these sensitive methods, 9 can be determined even in hair and sweat (94).…”

Section: Catabolism Of F-acidsmentioning

confidence: 99%

Furan fatty acids: Occurrence, synthesis, and reactions. Are furan fatty acids responsible for the cardioprotective effects of a fish diet?

Spiteller

2005

Lipids

150

170

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Furan FA (F-acids) are tri- or tetrasubstituted furan derivatives characterized by either a propyl or pentyl side chain in one of the alpha-positions; the other is substituted by a straight long-chain saturated acid with a carboxylic group at its end. F-acids are generated in large amounts in algae, but they are also produced by plants and microorganisms. Fish and other marine organisms as well as mammals consume F-acids in their food and incorporate them into phospholipids and cholesterol esters. F-acids are catabolized to dibasic urofuran acids, which are excreted in the urine. The biogenetic precursor of the most abundant F-acid, F6, is linoleic acid. Methyl groups in the beta-position are derived from adenosylmethionine. Owing to the different alkyl substituents, synthesis of F-acids requires multistep reactions. F-acids react readily with peroxyl radicals to generate dioxoenes. The radical-scavenging ability of F-acids may contribute to the protective properties of fish and fish oil diets against mortality from heart disease.

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“…The constellation of ESS is observed in a variety of clinical disorders, from carbohydrate deficiency, surgical intervention, liver or kidney failure, and in various situations encountered in intensive care unit patients (5)(6)(7). The etiopathogenesis of ESS is multi-factorial, based essentially on impaired T 4 binding to serum carrier proteins; it is caused by circulating inhibitors, such as indoxyl sulfate and hippuric acid (8). The decreased serum T 4 binding leads to reduced T 4 uptake from blood to tissues, and consequently to lower T 4 clearance rates (9).…”

Section: Introductionmentioning

confidence: 99%

Changes in metabolism of TRH in euthyroid sick syndrome

Duntas¹,

Nguyen²,

Keck³

et al. 1999

European Journal of Endocrinology

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Objective: The aim of this study was to examine the metabolism of a simple dose, intravenously administered TRH bolus of 200 mg, in patients with euthyroid sick syndrome (ESS). Patients and Methods:A TRH test was performed on ten ESS patients and ten controls upon admission (d1) and after recovery (d2). Blood samples were collected at 0, 10, 20 and 30 min after TRH injection. We analyzed the volume of distribution (V d ), the plasma clearance rate (PCR), the fractional clearance rate (FCR), the half-life (t 1=2 ) and the TSH response to the injection of TRH. Results: All patients had lower tri-iodothyronine (T 3 ) levels compared with controls (0:9 Ϯ 0:1 nmol/l vs 1:9 Ϯ 0:1 nmol/l; P < 0.0001; mean Ϯ S.D.; paired t-test). In addition, the V d (16:7 Ϯ 5:9/l vs 30:6 Ϯ 0:6/l; P < 0.0005) and PCR (2:0 Ϯ 0:80 l/min vs 3:3 Ϯ 0:25 l/min; P < 0.0005) were found statistically lowered in patients than in controls, whereas FCR (0:119 Ϯ 0:01 per min vs 0:110 Ϯ 0:01 per min; P < 0.025) was found increased in patients as opposed to controls. The t 1=2 of exogenously administered TRH was increased in ESS compared with controls (7:2 Ϯ 0:7 min vs 6:3 Ϯ 0:6 min; P < 0.005). TSH response to TRH was found significantly repressed at 10, 20 and 30 min after TRH injection. On d2, these findings had reverted to normal and no changes regarding the kinetics of TRH and the response of TSH could be detected between patients and controls. Conclusions:The results demonstrate an impairment of TRH metabolism in ESS. The findings may suggest altered enzymatic activity, responsible for TRH degradation in states of acute ESS. These changes might be involved in the pathogenesis of ESS and represent part of an adaptive mechanism to this syndrome.

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Hippuric acid and 3-car☐y-4-methyl-5-propyl-2-furanpropionic acid in serum and urine

Cited by 24 publications

References 22 publications

Small Molecule Metabolite Biomarker Candidates in Urine from Mice Exposed to Formaldehyde

Small Molecule Metabolite Biomarker Candidates in Urine from Mice Exposed to Formaldehyde

Furan fatty acids: Occurrence, synthesis, and reactions. Are furan fatty acids responsible for the cardioprotective effects of a fish diet?

Changes in metabolism of TRH in euthyroid sick syndrome

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