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At least 37 records · Page 2Linked to original sources
PubMed1998

Comparative study of reductive amination reaction on 5-(4-formyl-3,5-dimethoxyphenoxy)valeric acid and its monomethoxy analog using the Multipin approach.

The 5-(4-formyl-3,5-dimethoxyphenoxy)valeric acid (Barany) linker and its monomethoxy analog were applied to the Multipin method of solid phase synthesis. A comparative assessment of reductive amination and cleavage of these linkers under conditions of multiple synthesis indicated that both were applicable to a broad range of primary amines including aniline and 4-nitroaniline. Apart from the greater lability of the dimethoxy version under TFA cleavage, there was no observable advantage of one linker over the other within the described experiment.

Amination↗
PubMed1996

The utilization of 5-hydroxyl-2-amino valeric acid as a specific marker of oxidized arginine and proline residues in proteins.

Alteration of cellular proteins by oxidative modification could represent an important mechanism leading to cellular dysdifferentiation and age-related diseases. There is difficulty in testing this hypothesis because of a lack of specific assays that can measure the extent proteins are oxidized in nonpurified tissue preparations. Some methods used to measure carbonyl groups in nonpurified samples have serious limitations because of interference from other sources of carbonyl groups not being a product of oxidation-mediated damage. Oxidation of arginine and proline residues has been reported to produce gamma-glutamyl semialdehyde, which on reduction and acid hydrolysis, was predicted to form 5-hydroxy-2-amino valeric acid (HAVA). In this article we confirm this prediction using a GC/MS/SIM technique, and carry out additional experiments to determine if HAVA may be a useful marker of oxidative damage in proteins. These experiments utilized purified preparations of arginine, proline, histidine, and lysine amino acid homopolymers and six different purified proteins preparations in nonoxidized and oxidized states. Results demonstrate that HAVA compares well with the carbonyl group formation as a specific marker of oxidized protein, and that the GC/MS/SIM technique can detect HAVA reliably to 150 femtomoles per injection. Thus, HAVA as a specific marker of oxidized arginine and proline could prove to be a useful assay in pure and nonpurified samples.

Amino Acids↗
PubMed1993

The antiepileptic effect of low-dose amino-phosphono-valeric acid (APV) is not enhanced by phosphatidylserine association.

We investigated the effects of the NMDA antagonist amino-phosphono-valeric acid (APV), alone or in combination with phosphatidylserine (PS) in the penicillin model of epilepsy. After penicillin injection, rats were treated i.p. with either APV alone (5 mg/Kg) or APV (5 mg/Kg) + PS (740 mg/Kg). EEG epileptic activity decreased significantly in the group treated with APV alone, even at the very low dose used. This effect was not further enhanced by PS, suggesting that the previously reported effects of PS on GABA activity may be related to a specific interaction between these compounds.

2-Amino-5-phosphonovalerate↗
PubMed1980

Effect of azathioprine on antibody formation in mice and its modification by delta-(2-amino-6-hydroxy-3,4-dihydro-4-oxo-5-pyrimidinyl)-valeric acid.

The effects of azathioprine, either alone or combined with delta-(2-amino-6-hydroxy-3,4-dihydro-4-oxo-5-pyrimidinyl)-valeric acid (VUFB-9777, Damvar) on serum antibody formation was studied in mice. The immunosuppressive effect of azathioprine depended on the regimen of administration. VUFB-9777 alone produced no immunosuppressive effect but markedly enhanced that of azathioprine.

Animals↗
PubMed1996

Comparison of 5-hydroxy-2-amino valeric acid with carbonyl group content as a marker of oxidized protein in human and mouse liver tissues.

Previous studies indicate that 5-hydroxy-2-amino valeric acid (HAVA) is an excellent marker of oxidized arginine and proline in purified proteins. We report here experiments testing the specificity of the HAVA assay technique using the unpurified 100,000 x g supernatant fraction prepared from mice and human liver tissue. Results are compared to carbonyl group analysis on the same tissue samples. Mice at ages 3, 12, and 30 months were exposed to 100% oxygen. Results showed a significant increase of HAVA content in each age group. No significant changes were found in carbonyl group content. Because it has been reported that carbonyl group content increases with age, we applied the HAVA assay to reexamine this question. Using mice of 1 to 30 months of age, we failed to detect any significance difference in either HAVA or carbonyl group content. However, on using human liver samples a significant decrease from age 16 to 40 years and then an increase to 85 years of age was found for both HAVA and carbonyl groups. Liver proteins may be oxidized from hydrogen peroxide produced from the cytochrome P450 detoxification system. This possibility was supported by a significant positive correlation found between HAVA and cytochrome P450 content in 18 human individuals of different ages.

Aging↗
PubMed2005

Protective effect of alpha-keto-beta-methyl-n-valeric acid on BV-2 microglia under hypoxia or oxidative stress.

The alpha-ketoglutarate dehydrogenase complex (KGDHC) is a mitochondrial enzyme in the TCA cycle. Inhibition of KGDHC activity by alpha-keto-beta-methyl-n-valeric acid (KMV) is associated with neuron death. However, the effect of KMV in microglia is unclear. Therefore, we investigated the effect of KMV on BV-2 microglial cells exposed to hypoxia or oxidative stress. The results showed that KMV (1-20 mM) enhanced the cell viability under hypoxia. KMV dose-dependently reduced ROS and LDH releases from hypoxic BV-2 cells. KMV also reduced ROS production and enhanced the cell viability under H2O2 but failed to reduce the SIN-1 and sodium nitroprusside (SNP) toxicity. KMV also reduced caspase-3 and -9 activation under stress. These results suggest that KMV protects BV-2 cells from stress and acts by reducing ROS production through inhibition of KDGHC.

Apoptosis↗
PubMed2004

alpha-keto-beta-methyl-n-valeric acid diminishes reactive oxygen species and alters endoplasmic reticulum Ca(2+) stores.

Mitochondrial dysfunction and oxidative stress occur in neurodegenerative diseases. Other results show that bombesin-releasable calcium stores (BRCS) from the endoplasmic reticulum (ER) are exaggerated in fibroblasts from patients with Alzheimer's disease (AD) compared with controls and in fibroblasts from a young control treated with H(2)O(2). We hypothesize that alterations in oxidative stress underlie the exaggeration in BRCS in AD, and that appropriate antioxidants may be useful in treating this abnormality. Two indicators of different oxidant species were used to determine the effects of select oxidants on cellular oxidation status: carboxydichlorofluorescein (c-DCF) to detect reactive oxygen species (ROS), and 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF) to detect nitric oxide (NO(.-)). Various conditions that induce ROS, including H(2)O(2), oxygen/glucose deprivation, and 3-morpholinosyndnonimine (SIN-1), were used to test the ability of alpha-keto-ss-methyl-n-valeric acid (KMV) to scavenge ROS. KMV diminished c-DCF-detectable ROS that were induced by H(2)O(2), oxygen/glucose deprivation, or SIN-1 in PC12 cells, primary neuronal cultures, or fibroblasts. Furthermore, KMV reduced the H(2)O(2)-induced increase in BRCS and diminished the elevation in BRCS in cells from AD patients to control levels. On the other hand, DAF-detectable NO(.-) induced by SIN-1 was not scavenged by KMV and did not exaggerate BRCS. The results indicate that KMV is an effective antioxidant of c-DCF-detectable ROS. The effects of KMV are not cell type specific, but are ROS specific. The same H(2)O(2)-induced ROS that reacts with KMV may also underlie the changes in BRCS related to AD. Thus, KMV ameliorates the effects of ROS on calcium homeostasis related to oxidative stress and to AD.

Alzheimer Disease↗
PubMedDate not supplied

Synthesis of alpha-[7-methyl-9-methoxy-5-oxo-furo-[3,2-g] [1]-benzopyranoxy-4]-butyric and valeric acids and their aminoesters.

In the reaction of 4-desmethylkhelline with ethyl alpha-bromobutyrate or alpha-bromovalerate we obtained alpha-[7-methyl-9-methoxy-5-oxo-furo[3,2-g] [1] benzopyranoxy-4]-butyric 2 and valeric 3 acids and later their dialkylaminoethylesters as hydrochlorides (2b--2, 3b--3e). Compounds 2c, 2e, 2f (Table 1) and 3e (Table 2) show a weak hypotensic activity. Moreover compound 2f possesses an antriarrhythmic activity.

Aminobutyrates↗
PubMedDate not supplied

Transport kinetics of plasma free fatty acid, very low density lipoprotein triglycerides and apoprotein in patients with endogenous hypertriglyceridaemia: effects of 2,2-dimethyl, 5(2, 5-xylyoxy) valeric acid therapy.

The effects of C1-719 on plasma lipid and lipoprotein concentrations have been examined in four patients with endogenous hypertriglyceridaemia maintained on an isocaloric diet for a period of 6 months. During therapy (400 mg/day) the mean plasma triglyceride and cholesterol concentrations were reduced by 35% and 15% respectively, while the administration of 800 mg/day reduced these by 49% and 31%. This hypolipidaemic effect was due to a reduction in the circulating level of very low density lipoproteins (VLDL) without a change in their composition. Before treatment the plasma VLDL triglyceride turnover, and FFA flux, were higher than that of normal subjects maintained on a similar diet. The plasma VLDL B-apoprotein turnover was similarly higher than in the controls. Administration of C1-719 decreased the plasma VLDL triglyceride turnover, FFA flux and VLDL B-approtein turnover. The drug reduced the insulin response following a glucose load with some decrease in glucose levels. The results suggest that the increase in plasma triglyceride concentration in patients with endogenous hypertriglyceridaemia is due to increased production of plasma VLDL triglyceride and its apoptein associated with an enhanced supply of FFA for hepatic triglyceride synthesis. C1-719 exerts a hypolipidaemic effect through a reduction of VLDL production, consequent upon inhibition of lipolysis as well as decreased synthesis of the apoprotein carrier. These effects could in part be explained by an improvement in peripheral tissue responsiveness to insulin and decreased exposure of the liver to high levels of insulin. However, a direct effect of the drug on adipose tissue and liver metabolism has to be considered.

Adult↗