Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACIDS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed1990

Effects of halothane anaesthesia on extracellular levels of dopamine, dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindolacetic acid in rat striatum: a microdialysis study.

The effects of halothane anaesthesia on striatal extracellular levels of dopamine, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5HIAA) were investigated in microdialysis experiments. Induction of anaesthesia was accompanied by a rapid increase in dopamine levels and a slower increase in DOPAC and HVA. 5HIAA was not affected. The reduction of dopamine levels induced by apomorphine 0.05 mg/kg appeared with a shorter latency in conscious rats than in anaesthetised rats but the maximum decrease was unaffected by anaesthesia. The decreases in dopamine and DOPAC induced by alpha-methyl-p-tyrosine 50 mg/kg were affected in opposite directions by halothane: the dopamine reduction was more pronounced while the DOPAC reduction was less pronounced in anaesthetized than in conscious animals. In no case was a qualitative shift in the response observed. It is concluded that halothane may influence the levels of dopamine as well as the response to dopaminergic drugs.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Fatty acid metabolism and cell proliferation. III. Effect of prostaglandin biosynthesis either from exogenous fatty acid or endogenous fatty acid release with hydralazine.

Primary cultures of smooth muscle cells were established from the medial layer of guinea pig aorta. Cells were seeded at from 40 to 80 cells per cm2 and cloned for 8 days. Media were analyzed for PGI2 (6-keto-PGF1 alpha) using radioimmunoassay. Prostanoids were synthesized when cells were grown in media alone. Arachidonic acid stimulated prostanoid synthesis and promoted cell proliferation. Indomethacin blocked prostanoid synthesis and abolished the stimulatory effect of arachidonic acid on cell proliferation. Hydralazine stimulated fatty acid release and prostanoid synthesis in confluent cells. Hydralazine also stimulated prostanoid synthesis and promoted proliferation in growing cells. Indomethacin blocked prostanoid synthesis and abolished the stimulatory effect of hydralazine on cell proliferation.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

Low doses of eicosapentaenoic acid, docosahexaenoic acid, and hypolipidemic eicosapentaenoic acid derivatives have no effect on lipid peroxidation in plasma.

It was of interest to investigate the influence of both high doses of eicosapentaenoic acid (EPA) and low doses of 2- or 3-methylated EPA on the antioxidant status, as they all cause hypolipidemia, but the dose required is quite different. We fed low doses (250 mg/d/kg body wt) of different EPA derivatives or high doses (1500 mg/d/kg body wt) of EPA and DHA to rats for 5 and 7 d, respectively. The most potent hypolipidemic EPA derivative, 2,2-dimethyl-EPA, did not change the malondialdehyde content in liver or plasma. Plasma vitamin E decreased only after supplementation of those EPA derivatives that caused the greatest increase in the fatty acyl-CoA oxidase activity. Fatty acyl-CoA oxidase activity increased after administration of both EPA and DHA at high doses. High doses of EPA and DHA decreased plasma vitamin E content, whereas only DHA elevated lipid peroxidation. In liver, however, both EPA and DHA increased lipid peroxidation, but the hepatic level of vitamin E was unchanged. The glutathione-requiring enzymes and the glutathione level were unaffected, and no significant changes in the activities of xanthine oxidase and superoxide dismutase were observed in either low- or high-dose experiments. In conclusion, increased peroxisomal beta-oxidation in combination with high amounts of polyunsaturated fatty acids caused elevated lipid peroxidation. At low doses of polyunsaturated fatty acids, lipid peroxidation was unchanged, in spite of increased peroxisomal beta-oxidation, indicating that polyunsaturation is the most important factor for lipid peroxidation.

Acyl-CoA Oxidase↗
PubMed1984

Rapid and simple method for the simultaneous determination of 3,4-dihydroxyphenylacetic acid, 5-hydroxyindole-3-acetic acid and 4-hydroxy-3-methoxyphenylacetic acid in human plasma by high-performance liquid chromatography with electrochemical detection.

A simple procedure for the simultaneous determination of major metabolites of dopamine and serotonin in plasma, i.e. 3,4-dihydroxyphenylacetic acid, 5-hydroxyindole-3-acetic acid, and 4-hydroxy-3-methoxyphenylacetic acid, was developed. The method is based on rapid isolation of the compounds by one-step clean-up on a small C18 column, followed by high-performance liquid chromatography with dual electrochemical detection. The system is readily used for clinical applications.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Analysis of creatinine, vanilmandelic acid, homovanillic acid and uric acid in urine by micellar electrokinetic chromatography.

A simultaneous determination of vanilmandelic acid, homovanillic acid, creatinine and uric acid using capillary electrophoresis was investigated. The optimum conditions of buffer concentration, pH and surfactant concentration were studied, and high resolution was obtained using a 30 mM phosphate buffer (pH 7.0) containing 150 mM sodium dodecyl sulfate. The detection was by UV absorbance at 245 nm and the column was a fused-silica capillary of 67 cm x 75 microm I.D.. The determination of these metabolites in human urine was completed within 15 min without any interferences.

Buffers↗
PubMed1999

Simultaneous determination of gamma-aminobutyric acid and glutamic acid in the brain of 3-mercaptopropionic acid-treated rats using liquid chromatography-atmospheric pressure chemical ionization mass spectrometry.

The measurement of gamma-aminobutyric acid (GABA) and glutamic acid (Glu) in the whole brain and in various regions of the brain in 3-mercaptopropionic acid (3-MPA)-treated rats has been developed using liquid chromatography-mass spectrometry with an atmospheric pressure ionization interface system. The recoveries of these compounds were 94.90+/-4.18% for GABA, 95.60+/-2.86% for Glu after ion-exchange treatment. The detection limits for GABA and Glu were 2.5+/-0.3 microg/ml and 5.0+/-0.8 microg/ml, respectively, when 20 microl sample were injected. GABA concentration in the whole brain decreased gradually to 5 min and reached 63% of normal value after administration of 3-MPA, and the concentration increased gradually thereafter until 60 min. Conversely, the concentration of Glu in the whole brain increased gradually to 10 min and reached 154% of normal value, and after that decreased gradually and reached almost normal level at 60 min after administration of 3-MPA. GABA concentration in various regions of brain decreased to 5 min in all regions after administration of 3-MPA, and reached normal levels at 60 min as in the whole brain. This method was found to be useful for studies of metabolism of GABA and Glu in biological samples.

3-Mercaptopropionic Acid↗
PubMed2001

Covalent modification of glassy carbon electrode with glutamic acid for simultaneous determination of uric acid and ascorbic acid.

A novel covalently modified glassy carbon electrode with glutamic acid has been fabricated via an electrochemical oxidation procedure and was applied to the catalytic oxidation of uric acid (UA) and ascorbic acid (AA), reducing the overpotentials by about 0.2 V and 0.3 V, respectively. Based on its strong catalytic function toward the oxidation of UA and AA, the modified electrode resolved the overlapping voltammetric response of UA and AA into two well-defined voltammetric peaks with both cyclic voltammetry (CV) and differential pulse voltammetry (DPV), which can be used for the simultaneous determination of these species in a mixture. The catalytic peak current obtained from DPV was linearly dependent on the UA and AA concentration in the range 2 x 10(-6)-4 x 10(-4) mol L-1 and 1.0 x 10(-6)-4 x 10(-4) mol L-1 with correlation coefficients of 0.996 and 0.997, respectively. The detection limits (3 delta) for UA and AA were 1.1 x 10(-6) mol L-1 and 9.2 x 10(-7) mol L-1, respectively. The modified electrode shows good sensitivity, selectivity and stability, and has been applied to the determination of UA and AA simultaneously in human urine samples with satisfactory results.

Ascorbic Acid↗
PubMed1997

Differential role of homologous positively charged amino acid residues for ligand binding in retinoic acid receptor alpha compared with retinoic acid receptor beta.

The diverse biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARs) and retinoid X receptors. Although it has been suggested that the ligand binding domains (LBDs) of RARs share the same novel folding pattern, many RAR subtype-specific agonists and antagonists have been synthesized demonstrating that the LBD of each RAR subtype has unique features. We have examined the role of several positively charged amino acid residues located in the LBD of RARalpha in RA binding. These results are compared with previously published data for the homologous mutations in RARbeta. Lys227 of RARalpha does not appear to be important for RA binding or RA-dependent transactivation, whereas the homologous residue in RARbeta, Lys220, plays an important synergistic role with Arg269 in these two activities. In addition, Arg276 of RARalpha, like its homologous residue Arg269 of RARbeta, was found to play an important role in the binding of RA most likely by interacting with the carboxylate group of RA. However, the orientation of and electronic environment associated with Arg276 in RARalpha appears to be different from that of Arg269 in RARbeta, thus contributing to the uniqueness of the ligand binding pocket of each receptor.

Amino Acids, Diamino↗
PubMed1994

Prevention by acetylsalicylic acid of liver cirrhosis and carcinogenesis as well as generations of 8-hydroxydeoxyguanosine and thiobarbituric acid-reactive substances caused by a choline-deficient, L-amino acid-defined diet in rats.

Effects of acetylsalicylic acid (ASA) (aspirin) on the pathogenesis of fatty liver, cirrhosis and hepatocarcinogenesis caused by a choline-deficient L-amino acid-defined (CDAA) diet were examined in male Fischer 344 rats fed a CDAA diet supplemented with 0, 0.1, 0.2, 0.4 or 0.8% ASA for 30 weeks. ASA at concentrations of > 0.2% prevented the development of both cirrhosis and preneoplastic and neoplastic nodules, but without any directly associated prevention of fatty changes. ASA also prevented hepatocyte proliferation and the generation of thiobarbituric acid-reactive substances and 8-hydroxydeoxyguanosine caused by feeding the CDAA diet, analyzed, respectively, after 1, 12 and 12 weeks. The results clearly indicate that the anti-inflammatory drug ASA, which is not a lipotropic factor, can prevent the pathogenesis of cirrhosis and hepatocarcinogenesis caused by a CDAA diet, which is possibly partly associated with the prevention of reactive oxygen species production.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1998

Differential effects of 1-naphthaleneacetic acid, indole-3-acetic acid and 2,4-dichlorophenoxyacetic acid on the gravitropic response of roots in an auxin-resistant mutant of arabidopsis, aux1.

The agravitropic nature of root growth of an auxin-resistant mutant of Arabidopsis, aux1, was restored when the synthetic auxin 1-naphthaleneacetic acid (NAA) was added to the growth medium; aux1 roots were not resistant to NAA. Neither indole-3-acetic acid nor, 2,4-dichlorophenoxyacetic acid had the same effects as NAA. These differential effects of the three auxins on aux1 defects suggest that AUX1 may encode the auxin influx carrier according to the model proposed by Delbarre et al.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2003

Restoration of defective cross talk in ssi2 mutants: role of salicylic acid, jasmonic acid, and fatty acids in SSI2-mediated signaling.

The Arabidopsis mutants ssi2 and fab2 are defective in stearoyl ACP desaturase, which causes altered salicylic acid (SA)- and jasmonic acid (JA)-mediated defense signaling. Both ssi2 and fab2 plants show spontaneous cell death, express PR genes constitutively, accumulate high levels of SA, and exhibit enhanced resistance to bacterial and oomycete pathogens. In contrast to constitutive activation of the SA pathway, ssi2 and fab2 plants are repressed in JA-mediated induction of the PDF1.2 gene, which suggests that the SSI2-mediated signaling pathway modulates cross talk between the SA and JA pathways. In this study, we have characterized two recessive nonallelic mutants in the ssi2 background, designated as rdc (restorer of defective cross talk) 2 and rdc8. Both ssi2 rdc mutants are suppressed in constitutive SA signaling, show basal level expression of PR-1 gene, and induce high levels of PDF1.2 in response to exogenous application of JA. Interestingly, while the rdc8 mutation completely abolishes spontaneous cell death in ssi2 rdc8 plants, the ssi2 rdc2 plants continue to show some albeit reduced cell death. Fatty acid (FA) analysis showed a reduction in 16:3 levels in ssi2 rdc8 plants, which suggests that this mutation may limit the flux of FAs into the prokaryotic pathway of glycerolipid biosynthesis. Both rdc2 and rdc8 continue to accumulate high levels of 18:0, which suggests that 18:0 levels were responsible for neither constitutive SA signaling nor repression of JA-induced expression of the PDF1.2 gene in ssi2 plants. We also analyzed SA and JA responses of the fab2-derived shs1 mutant, which accumulates levels of 18:0 over 50% lower than those in the fab2 plants. Even though fab2 shs1 plants were morphologically bigger than fab2 plants, they expressed PR genes constitutively, showed HR-like cell death, and accumulated elevated levels of SA. However, unlike the ssi2 rdc plants, fab2 shs1 plants were unable to induce high levels of PDF1.2 expression in response to exogenous application of JA. Together, these results show that defective cross talk in ssi2 can be restored by second site mutations and is independent of morphological size of the plants, cell death, and elevated levels of 18:0.

Arabidopsis↗
PubMedDate not supplied

Human seminal biochemistry: fructose, ascorbic acid, citric acid, acid phosphatase and their relationship with sperm count.

Seminal concentration of fructose, ascorbic acid, citric acid and acid phosphatase were measured in azoospermic, oligozoospermic and control males. No significant differences were found among the groups evaluated. The data obtained in the present study suggest that in the absence of infection and androgen deficiency, the failure of the germinal line of the testis is not correlated with alterations of the adnexal glands.

Acid Phosphatase↗