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PubMed1991

Simultaneous analysis of flunixin, naproxen, ethacrynic acid, indomethacin, phenylbutazone, mefenamic acid and thiosalicylic acid in plasma and urine by high-performance liquid chromatography and gas chromatography-mass spectrometry.

Simple and reproducible high-performance liquid chromatographic (HPLC) and gas chromatographic-mass spectrometric (GC-MS) methods have been developed for the simultaneous analysis of several acidic drugs in horse plasma and urine. Although the capillary GC-MS column provided better separation of the drugs than the reversed-phase C8 (3 microns, 75 mm) HPLC column, the total analysis time with HPLC was shorter than the total analysis time with GC-MS. The HPLC system equipped with a diode-array detector provided simultaneous screening (limit of detection 100-500 ng/ml) and confirmation (limit 1.0 micrograms/ml) of the drugs. The HPLC system equipped with fixed-wavelength ultraviolet and fluorescence detectors provided a relatively sensitive screening [limit of detection 50-150 ng/ml for ultraviolet and 10 ng/ml for fluorescence (naproxen only) detectors] of the drugs. However, the positive samples had to be confirmed by using either the diode-array detector or the GC-MS system. The GC-MS system provided simultaneous screening and confirmation of the drugs at very low concentrations (20-50 ng/ml).

Analgesics↗
PubMed1978

Mass fragmentographic determination of vanilmandelic acid, homovanillic acid and isohomovanillic acid in human body fluids.

Vanilmandelic, homovanillic and isohomovanillic acids in body fluids were efficiently isolated by liquid chromatography on an Amberlite XAD-4 column and by organic extraction in a special apparatus. The purified metabolites were converted into their trifluoroacetylhexafluroisopropanol esters and analyzed by mass fragmentography. The working curves of the metabolites were linear from 0.5 to 5 ng injected. The minimum detectable concentrations of all the metabolites were 2 ng/ml for plasma and cerebrospinal fluid, and 120 ng/ml for urine. The metabolite concentrations in plasma, cerebrospinal fluid and urine of normal persons and patients were determined.

Adolescent↗
PubMed1998

Retinoic acid receptors regulate expression of retinoic acid 4-hydroxylase that specifically inactivates all-trans retinoic acid in human keratinocyte HaCaT cells.

Tissue levels of all-trans retinoic acid (RA) are maintained through coordinated regulation of biosynthesis and breakdown. The major pathway for all-trans RA inactivation is initiated by 4-hydroxylation. A novel cytochrome P-450 (CYP26) that catalyzes 4-hydroxylation of all-trans RA has recently been cloned. We have investigated regulation and properties of RA 4-hydroxylase in immortalized human keratinocyte HaCaT cells. In the absence of added retinoid, RA 4-hydroxylase (CYP26) mRNA and protein were minimally detected. Addition of all-trans RA rapidly induced RA 4-hydroxylase mRNA (within 2 h) and activity (within 6 h). Induction of both mRNA and activity was transient, returning to baseline within 48 h, and completely dependent on mRNA synthesis (i.e., blocked by actinomycin D). The synthetic retinoid CD367, which specifically activates nuclear RA receptors, also rapidly induced RA 4-hydroxylase activity. This induction, however, unlike that of all-trans RA, was long-lived (>48 h). This difference was attributable to lack of metabolic inactivation of CD367 in HaCaT cells. CD2665, which inhibits RA receptor-dependent gene transcription, blocked retinoid induction of RA 4-hydroxylase, indicating that it is mediated by RA receptors. Addition of excess unlabeled substrates specific for 10 distinct mammalian P-450 subfamilies did not compete with all-trans RA for RA 4-hydroxylase activity. RA 4-hydroxylase did not hydroxylate 9-cis RA or 13-cis RA. Inhibition of RA 4-hydroxylase activity by ketoconazole potentiated activation of RA receptors by all-trans RA. In summary, RA 4-hydroxylase is a unique, highly specific cytochrome P-450 isoenzyme, whose expression is regulated by its natural substrate, all-trans RA, through activation of RA receptors. RA 4-hydroxylase functions to limit the levels, and thereby the biologic activity of all-trans RA in HaCaT cells.

Alitretinoin↗
PubMed1986

Respective contribution of plasma branched-chain amino acids and 2-keto acids to the hepatic metabolism of the carbon moiety of branched-chain amino acids in fed rats.

The splanchnic balances of branched-chain amino acids (BCAA) and ketoacids (BCKA) concentrations were compared in rats fed a 15% (basal) or a 70% (HP) casein diet. Arterial BCAA concentrations were four- to fivefold and BCKA concentrations were twofold higher in rats fed HP diet than in rats fed basal diet. In rats fed basal diet, a higher proportion (45-58%) of BCKA was removed by the liver than of BCAA (7-12%). Thus, plasma BCKA were probably the major source of substrates for hepatic BCKA dehydrogenase. In rats fed HP diet, hepatic uptake of BCAA was 10 times greater than in rats fed basal diet, owing to their higher extraction; BCKA uptake was only twice as great; thus BCKA were a minor source of substrates for hepatic metabolism. In both diet groups, uptake of ketomethylvalerate (KMV) was less efficient than ketoisovalerate (KIV) or ketoisocaproate (KIC) uptake. Studies of metabolism of intraportal loads of BCKA showed that capacities for KIV and KIC uptake were high, KMV uptake plateaued at lower portal concentrations. With HP diets, the liver may be the major site of BCAA utilization; the interorgan transfer of the carbon moiety of BCAA to the liver as ketoacids does not keep pace with an increased availability of BCAA.

Amino Acids, Branched-Chain↗
PubMed2002

Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake.

Sulfo-N-succinimidyl esters of LCFAs are a powerful tool to investigate the functional significance of plasmalemmal proteins in the LCFA uptake process. This notion is based on the following observations. First, sulfo-N-succinimidyl oleate (SSO) was found to inhibit the bulk of LCFA uptake into various cell types, i.e. rat adipocytes, type II pneumocytes and cardiac myocytes. Second, using cardiac giant membrane vesicles, in which LCFA uptake can be investigated in the absence of mitochondrial beta-oxidation, SSO retained the ability to largely inhibit LCFA uptake, indicating that inhibition of LCFA transsarcolemmal transport is its primary action. Third, SSO has no inhibitory effect on glucose and octanoate uptake into giant membrane vesicles derived from heart and skeletal muscle, indicating that its action is specific for LCFA uptake. Finally, SSO specifically binds to the 88 kDa plasmalemmal fatty acid transporter FAT, a rat homologue of human CD36, resulting in an arrest of the transport function of this protein. In addition to its inhibitory action at the plasma membrane level, evidence is presented for the lack of a direct inhibitory effect on subsequent LCFA metabolism. First, the relative contribution of oxidation and esterification to LCFA uptake is not altered in the presence of SSO. Second, isoproterenol-mediated channeling of LCFAs into oxidative pathways is not affected by sulfo-N-succinimidyl palmitate (SSP). As an example of its application, we used SSP to study the role of FAT/CD36 in contraction- and insulin-stimulated LCFA uptake by cardiac myocytes, showing that this transporter is a primary site of regulation of cellular LCFA utilization.

Animals↗
PubMed2004

Conversion regular patterns of acetic acid, propionic acid and butyric acid in UASB reactor.

On the basis of continuous tests and batch tests, conversion regular patterns of acetate, propionate and butyrate in activated sludge at different heights of the UASB reactor were conducted. Results indicated that the conversion capacity of the microbe is decided by the substrate characteristic when sole VFA is used as the only substrate. But when mixed substrates are used, the conversion regulations would have changed accordingly. Relationships of different substrates vary according to their locations. In the whole reactor, propionate's conversion is restrained by acetate and butyrate of high concentration. On the top and at the bottom of the reactor, conversion of acetate, but butyrate, is restrained by propionate. And in the midst, acetate's conversion is accelerated by propionate while that of butyrate is restrained. It is proved, based on the analysis of specific conversion rate, that the space distribution of the microbe is the main factor that affects substrates' conversion. The ethanol-type fermentation of the acidogenic-phase is the optimal acid-type fermentation for the two-phase anaerobic process.

Acetic Acid↗
PubMed1992

Configuration of the 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholest-24-enoic acid, an intermediate in the peroxisomal conversion of 3 alpha,7 alpha,12-trihydroxy-5 beta-cholestanoic acid to cholic acid in rat liver.

3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholest-24-enoic acid, formed in the peroxisomal oxidation of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoyl-CoA by the THCA-CoA oxidase in rat liver, was isolated and purified on reverse phase HPLC. The configuration of the C-24/25 double bond was determined to be trans (E) by using 1H-NMR spectrometry.

Animals↗
PubMed1989

Defective lysosomal egress of free sialic acid (N-acetylneuraminic acid) in fibroblasts of patients with infantile free sialic acid storage disease.

Egress of free NeuAc from normal lysosome-rich granular fractions was assessed at NeuAc concentrations of up to 221 pmol/hexosaminidase unit, achieved by exposure of growing fibroblasts to 40-125 nM N-acetylmannosamine for up to 7 days. The normal velocity of NeuAc egress increased with NeuAc loading and with temperature, exhibiting a Q10 of 2.4, characteristic of carrier-mediated transport. Fibroblasts cultured from five patients with infantile free sialic acid storage disease (ISSD) contained approximately 139 nmol of free NeuAc/mg of whole cell protein, or 100 times the normal level. Differential centrifugation, as well as density gradient analysis using 25% Percoll, showed that the stored NeuAc cosedimented with the lysosomal enzyme beta-hexosaminidase. The velocity of appearance of free NeuAc outside ISSD granular fractions was negligible, even at initial loading levels of up to 3500 pmol/hexosaminidase unit. The lack of egress from ISSD granular fractions was found for both endogenous and N-acetylmannosamine-derived NeuAc. Fibroblasts from ISSD parents did not accumulate excess free NeuAc and did not display a velocity of NeuAc egress significantly different from normal. The defect in ISSD, like that in Salla disease, appears to be an impairment of carrier-mediated transport of free NeuAc across the lysosomal membrane. Clinical and biochemical differences between Salla disease and ISSD may reflect differences in the amount of residual NeuAc transport capacity.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1989

Characterization of serum and urinary bile acids in patients with primary biliary cirrhosis by gas-liquid chromatography-mass spectrometry: effect of ursodeoxycholic acid treatment.

We have studied the effect of ursodeoxycholic acid on the serum and urinary bile acids in seven patients with moderate to severe primary biliary cirrhosis. Bile acids were characterized by gas-liquid chromatography-mass spectrometry and quantified by capillary gas-liquid chromatography. Serum bile acids were elevated 26-fold over control values, with 2.2 times more cholic acid than chenodeoxycholic acid. Urinary bile acid output was elevated 22-fold over control values with a cholic acid:chenodeoxycholic acid ratio of 1.6. In addition, lithocholic acid, deoxycholic acid, ursodeoxycholic acid, 1 beta-hydroxycholic acid, 1 beta-hydroxydeoxycholic acid, and hyocholic acid were identified in both serum and urine; the proportions of the 1- and 6-hydroxylated bile acids were much higher in urine than in serum of the patients (32.1% versus 4.2%). Three months of placebo administration did not change the serum and urinary bile acid composition. In contrast, ursodeoxycholic acid feeding (12-15 mg/kg body weight per day) for 6 months resulted in a 25% decline in the total serum bile acid concentration from the pretreatment values. The proportion of ursodeoxycholic acid increased from 2.1 to 41.2% of total bile acids, so that total fasting serum endogenous bile acid levels decreased 62.4%. Ursodeoxycholic acid feeding substantially increased urinary bile acid output, with ursodeoxycholic acid comprising 58.1%. The proportion of 1- and 6- hydroxylated endogenous bile acids was reduced by 45.5% from pretreatment levels and approximately 4.5% of the urinary bile acids were omega-muricholic acid, 1 beta-hydroxyursodeoxycholic acid, and 21-hydroxyursodeoxycholic acid. These results demonstrate significant changes in the serum and urinary bile acid pattern in primary biliary cirrhosis during ursodeoxycholic acid treatment. The beneficial effect of ursodeoxycholic acid may be due to reduction of the hydroxylated derivatives of endogenous bile acids together with the appearance of hydroxylated derivatives of ursodeoxycholic acid or it may be due to displacement of the more hydrophobic endogenous bile acids by the hydrophilic ursodeoxycholic acid.

Bile Acids and Salts↗
PubMed1982

The origin of urinary aromatic compounds excreted by ruminants. 1. The metabolism of quinic, cyclohexanecarboxylic and non-phenolic aromatic acids to benzoic acid.

1. The contribution of dietary constituents to the large urinary output of benzoic acid characteristic of ruminants and some herbivores is not well understood. 2. Methods for the analysis of quinic, cyclohexanecarboxylic, benzoic, phenylacetic, 3-phenylpropionic and cinnamic acids in urine and in rumen fluids were developed. 3. The urinary output of aromatic acids by sheep given seven-rations was determined: benzoic acid output varied between 2.8 and 7.8 g/d; phenylacetic acid output between 0.16 and 1.3 g/d; cinnamic acid between 0.08 and 0.25 g/d and small amounts of 3-phenylpropionic acid were found in some samples. 4. Increments in urinary aromatic acid excretion were determined when the acids listed in paragraph 2 were infused via rumen or abomasal cannulas. 5. When cyclohexanecarboxylic acid was infused 40% of the dose was excreted as urinary benzoic acid after either route of infusion. Quinic acid was completely metabolized in the rumen; following rumen infusion between 16 and 53% of the infused acid was recovered as urinary benzoic acid; none was so recovered after abomasal infusion. 6. Urinary recoveries of rumen- and abomasally-infused aromatic acids were: benzoic acid 90 and 88% respectively as benzoic acid, phenylacetic acid 78 and 83% respectively as phenylacetic acid, 3-phenylpropionic acid 96 and 105% respectively as benzoic acid and cinnamic acid, 70 and 70% respectively as benzoic acid. 7. The concentration of aromatic acids in rumen fluid varied with time after feeding: cyclohexanecarboxylic acid was maximal (7 mg/l) 1 h after feeding, benzoic acid was always a minor component (0.5 +/- 0.5 mg/l), phenylacetic acid varied between 0 and 35 mg/l and 3-phenylpropionic acid between 25 and 47 mg/l. Cinnamic acid was not found in rumen fluid but on rumen infusion of this acid the concentration of 3-phenylpropionic acid in rumen fluid increased by 10 mg/l rumen fluid per g infused per d. 8. The incomplete metabolism of quinic and cyclohexanecarboxylic acids to urinary benzoic acid is discussed. It is concluded that the principal dietary precursors of urinary benzoic acid in ruminants are compounds yielding 3-phenylpropionic acid on microbial fermentation in the rumen. The small amount of cinnamic acid characteristic of ruminant urine arises as an intermediate in the beta-oxidation of 3-phenylpropionic acid in the body tissues.

Animal Feed↗
PubMed1996

Effect of dietary linoleic, alpha-linolenic and arachidonic acids on lipid metabolism, tissue fatty acid composition and eicosanoid production in rats.

Rats were fed semipurified diets containing 10% fat with a constant polyunsaturated/monounsaturated/saturated fatty acid ratio of 1:1:1. This was performed by mixing vegetable oils. Linoleic acid was the sole polyunsaturated fatty acid in the linoleic acid group. The alpha-linolenic and arachidonic acids were contained at the 1% level in the diet at the expense of linoleic acid in the alpha-linolenic acid and arachidonic acid groups, respectively. The concentration of serum triglyceride, phospholipid and liver triglyceride were significantly lower in the alpha-linolenic acid and arachidonic acid groups than in the linoleic acid group. Hepatic phospholipids were significantly higher in the alpha-linolenic acid and arachidonic acid group as compared to the linoleic acid group. Compared to the linoleic acid group, the percentages of arachidonic acid in the phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in the liver and heart were significantly lower in the alpha-linolenic acid group; in contrast, they were significantly higher in the arachidonic acid group. Dietary arachidonic acid, but not alpha-linolenic acid, resulted in a marked reduction of linoleic acid and increased arachidonic and n-6 docosapentaenoic acids in heart cardiolipin. Platelet thromboxane (TX) A2 production tended to be lower in the alpha-linolenic acid group as compared to the linoleic acid and arachidonic acid groups. There was no difference in TXA2 production between the linoleic acid and arachidonic acid groups. The aortic production of prostacyclin (PGI2) was the same among the three groups. The ratios of TXA2 and PGI2 in the linoleic acid and arachidonic acid groups were comparable, whereas they were significantly higher than that in the alpha-linolenic acid group. The results demonstrate that dietary arachidonic acid enriches the arachidonic acid content in tissue phospholipids more effectively than linoleic acid, whereas the effect on the production of TXA2 and PGI2 was comparable under these experimental conditions.

Animals↗
PubMed1990

Transport, metabolism, and effect of chronic feeding of lagodeoxycholic acid. A new, natural bile acid.

Ursodeoxycholic acid, the 7 beta-hydroxy epimer of chenodeoxycholic acid, is more hydrophilic and less hepatotoxic than chenodeoxycholic acid. Because "lagodeoxycholic acid," the 12 beta-hydroxy epimer of deoxycholic acid, is also more hydrophilic than deoxycholic acid, it was hypothesized that it should also be less hepatotoxic than deoxycholic acid. To test this, lagodeoxycholic acid was synthesized, and its transport and metabolism were examined in the rat, rabbit, and hamster. The taurine conjugate of lagodeoxycholic acid was moderately well transported by the perfused rat ileum (Tmax = 2 mumol/min.kg). In rats and hamsters with biliary fistulas, the taurine conjugate of lagodeoxycholic acid was well transported by the liver with a Tmax greater than 20 mumol/min.kg; for the taurine conjugate of deoxycholic acid, doses infused at a rate greater than 2.5 mumol/min.kg are known to cause cholestasis and death. Hepatic biotransformation of lagodeoxycholic acid in the rabbit was limited to conjugation with glycine; in the hamster, lagodeoxycholic acid was conjugated with glycine or taurine; in addition, 7-hydroxylation occurred to a slight extent (approximately 10%). When lagodeoxycholic acid was instilled in the rabbit colon, it was absorbed as such although within hours it was progressively epimerized by bacteria to deoxycholic acid. When injected intravenously and allowed to circulate enterohepatically, lagodeoxycholic acid was largely epimerized to deoxycholic acid in 24 hours. Surgical creation of a distal ileostomy abolished epimerization in the rabbit, indicating that exposure to colonic bacterial enzymes was required for the epimerization. Lagodeoxycholic acid was administered for 3 weeks at a dose of 180 mumol/day (0.1% by weight of a chow diet; 2-4 times the endogenous bile acid synthesis rate); other groups received identical doses of deoxycholic acid (hamster) or cholyltaurine, a known precursor of deoxycholic acid (rabbit). After 3 weeks of lagodeoxycholic acid ingestion, liver test results and liver appearance were normal. The total bile acid pool expanded by 37% in the rabbit, lagodeoxycholic acid composing 10% of biliary bile acids. In the hamster, the total bile acid pool was expanded by 95%, lagodeoxycholic acid composing 22% of biliary bile acids; biliary lipid secretion remained unchanged. Tracer studies indicated that the fractional turnover rate of lagodeoxycholic acid was high (157%/day, rabbit; 116%/day, hamster) because of its rapid epimerization to deoxycholic acid in the colon. These studies indicate that lagodeoxycholic acid, the more hydrophilic epimer of deoxycholic acid, is transported and metabolized as other dihydroxy bile acids but is much less toxic than deoxycholic acid.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

Studies on the oxidation of phytanic acid and pristanic acid in human fibroblasts by acylcarnitine analysis.

The alpha-oxidation of phytanic acid and the beta-oxidation of pristanitc acid were investigated in cultured fibroblasts from controls and patients affected with different peroxisomal disorders using deuterated substrates. Formation of [omega-2H6]4,8-dimethylnonanoylcarnitine ([omega-2H6]C11-carnitine) from [omega-2H6]phytanic acid and [omega-2H6]pristanic acid was used as marker for these processes. Analysis was performed by tandem mass spectrometry. In normal cells, formation of [omega-2H6]C11-carnitine from both [omega-2H6]phytanic acid and [omega-2H6]pristanic acid was observed. When peroxisome-deficient fibroblasts were incubated with these substrates, [omega-2H6]C11-carnitine was not detectable or, in two cases, very low, which results from deficiencies in both peroxisomal alpha- and beta-oxidation. In cells with an isolated beta-oxidation defect at the level of the peroxisomal bifunctional protein, formation of [omega-2H6]C11-carnitine could also not be detected. Cells with an isolated defect in the alpha-oxidation of phytanic acid, obtained from patients affected with Refsum disease (McKusick 266500) or rhizomelic chondrodysplasia punctata (McKusick 215100), did not form [omega-2H6]C11-carnitine from [omega-2H6]phytanic acid. The observed formation of [omega-2H6]C11-carnitine from [omega-2H6]pristanic acid in these cells is in accordance with a normal peroxisomal beta-oxidation in these disorders. This study shows that separate incubation of fibroblasts with [omega-2H6]phytanic acid and [omega-2H6]pristanic acid, followed by acylcarnitine analysis in the medium by tandem mass spectrometry, can be used for screening cell lines for deficiencies in the peroxisomal alpha- and beta-oxidation pathways. Phytanic acid (3,7,11,15-tetramethylhexadecanoic acid) and pristanic acid (2,6,10,14-tetramethylpentadecanoic acid) are branched-chain fatty acids that are constituents of the human diet. As phytanic acid possesses a beta-methyl group, it cannot be degraded by beta-oxidation. Instead, phytanic acid is first degraded by alpha-oxidation, yielding pristanic acid, which is subsequently degraded by beta-oxidation (Figure 1). Phytanic acid alpha-oxidation is thought to occur partly, and pristanic acid beta-oxidation exclusively, in peroxisomes (see Wanders et al 1995 for review). Accumulation of phytanic acid and pristanic acid is found in blood and tissues of patients affected with generalized peroxisomal disorders. In this type of disorder, no morphologically distinguishable peroxisomes are present in tissues, resulting in accumulation of metabolites that are normally metabolized in these organelles (see Wanders et al 1995 for review). The group of generalized peroxisomal disorders consists of three diseases, differing in clinical presentation. Patients suffering from the most severe disease, Zellweger syndrome (McKusick 214100), have symptoms from birth on and usually do not live beyond their first year of life. Neonatal adrenoleukodystrophy (N-ALD, McKusick 202370) has a milder presentation, whereas infantile Refsum disease (IRD, McKusick 266510) is the mildest form among the generalized peroxisomal disorders. Not only in these generalized peroxisomal disorders, but also in some isolated peroxisomal beta-oxidation defects, elevated levels of phytanic acid and pristanic acid are found (ten Brink et al 1992a). The elevated phytanic acid levels are considered to be caused by product inhibition of alpha-oxidation by accumulating pristanic acid. This is reflected in a highly elevated pristanic acid to phytanic acid ratio in plasma from patients suffering from bifunctional protein deficiency or peroxisomal thiolase deficiency (ten Brink et al 1992a). Elevated phytanic acid concentrations are also found in plasma from patients affected with classical Refsum disease and rhizomelic chondrodysplasia punctata (RCDP). As pristanic acid beta-oxidation is not disturbed in these disorders, pristanic acid levels are normal (ten Brink et al 1992

Carnitine↗