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PubMed1975

Separation of two L-glutamine-hydroxylamine glutamyltransferases from rat liver.

The purification of glutamine synthetase (GS) from rat liver demonstrates that a small portion of glutamine-hydroxylamine-glutamyltransferase activity (GT) remains associated with GS activity (GT(S)). As GS is purified from the water extract, the ratio between GT(S) activity (GT(T)) is left to be extracted by KC1 from the pellet and, on further purification, appears to be independent of GS activity. Subtle differences in pH optimum, substrate requirement and reaction rates on addition of cofactors and amino acids in vitro and in responses to hormonal stimuli in vivo indicate that the glutamine transfer reaction may be catalyzed by two distinguishable proteins; only the minor component may be identical to GS.

Acyltransferases↗
PubMed2005

N-t-Butyl hydroxylamine regulates heat shock-induced apoptosis in U937 cells.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Therefore, compounds that scavenge reactive oxygen species may regulate heat shock-induced cell death. Recently, it has been shown that the decomposition product of the spin-trapping agent alpha-phenyl-N-t-butylnitrone, N-t-butyl hydroxylamine (NtBHA), mimics alpha-phenyl-N-t-butylnitrone and is much more potent in delaying reactive oxygen species-associated senescence. We investigated the protective role of NtBHA against heat shock-induced apoptosis in U937 cells. Upon exposure to heat shock, there was a distinct difference between the untreated cells and the cells pre-treated with 0.1 mM NtBHA for 2 h in regard to apoptotic parameters, cellular redox status, and mitochondrial function. Upon exposure to heat shock, NtBHA pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax, and down-regulation of Bcl-2 compared to untreated cells. This study indicates that NtBHA may play an important role in regulating the apoptosis induced by heat shock, presumably through scavenging of reactive oxygen species.

Apoptosis↗
PubMedDate not supplied

Superoxide-dependent and -independent nitrite formation from hydroxylamine: inhibition by plant extracts.

Reactive oxygen species such as OH, peroxynitrite and the non-radical, hypochlorous acid, play outstanding roles in many disease. The formation of OH (Fenton)-type radicals is catalyzed by enzymes such as xanthine oxidase (XOD) via one-electron reduction of molecular oxygen producing superoxide radical anions (O2). Subsequent transfer of one electron to hydrogen peroxide by Fe2+ or Cu+ -ions yields OH-radicals measurable as ethene release from 1-keto-4-methylthiobutyrate (KMB). Xanthine oxidase or activated neutrophils are prominent sources of this strong oxidant produced at inflammatory sites. Many natural compounds such as salicylates or flavonoids interfere either with the production of these activated oxygen species or function as radical scavengers and thus as antioxidants. Extracts from willow-bark (Salix spec.) and also other species such as ash-tree (Fraxinus spec.) or poplar (Populus spec.) have been used as antiinflammatory drugs since a long time. In this communication we wish to report on model reactions to demonstrate a) the radical scavenging activities of such plant extracts inhibiting ethene release from KMB induced by Fenton-type oxidants and b) the inhibition of the formation of nitrogen monoxide (NO) from hydroxylamine including XOD either in the presence or absence of myoglobin (MYO) measurable as nitrite formation: In the absence of MYO, superoxide dismutase is an excellent inhibitor of nitrite formation but is inactive in its presence. Extracts from the willow-bark or the drug Phytodolar however, are inhibitory both in the presence and absence of MYO. As active principle, the flavonoid rutin included in these extracts is likely to function as one inhibitor of the XOD-mediated reaction.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Hemolytic potential of structurally related aniline halogenated hydroxylamines.

This study was undertaken to investigate the hemolytic potential of several structurally related aniline halogenated phenylhydroxylamines based on their decreasing electro negativity. The compounds compared are phenylhydroxylamine (PHA) and para-fluoro-, para-bromo-, and para-iodo-phenylhydroxylamines. Red blood cells of male Sprague-Dawley rats were labeled with radioactive chromium-51 and exposed to the test agent before being infused into the tail vein of isologous rats. The time course of blood radioactivity was monitored. The stability of some selected halogenated aniline analogs was also determined in blood. All four tested hydroxylamines produced dose-dependent reduction in the circulating labeled red blood cells indicating their destruction and loss. The most pronounced reduction was observed at doses from 175 to 250 microM. The dose of 100 microM appeared to be the threshold limit. The para-iodo-PHA was two times more toxic than para-fluoro-PHA in the destruction of red blood cells in rats.

Anemia, Hemolytic↗
PubMed1989

Reactions between dipeptidyl peptidase IV and diacyl hydroxylamines: mechanistic investigations.

Kinetics of inactivation of dipeptidyl peptidase IV (DP IV, EC 3.4.14.5) by N-peptidyl-O-(4-nitrobenzoyl) hydroxylamines and their enzyme-catalyzed hydrolysis were followed using independent monitoring methods, all giving similar efficiency ratios of Kcat/Kinact. Different temperature dependences of the DP IV-inactivation and enzyme-catalyzed hydrolysis provide evidence of independent rate determining steps for both reactions. Activation parameters of inactivation are similar to those of spontaneous decomposition of the compounds, suggesting a mechanistic relationship. Investigation of DP IV-inactivation, DP IV-catalyzed hydrolysis of N-Ala-Pro-O-Bz(4-NO2) and the decomposition of the suicide substrate in H2O and D2O gave solvent isotope effects of 4.65, 2.54 and 1.02, respectively. A proton inventory of the inactivation reaction indicates involvement of more than one proton in the formation or breakdown of its transition state. The linear proton inventory found for the hydrolytic reaction is consistent with one proton transition in the rate determining step and resembles the rate limiting deacylation of Ala-Pro-DP IV. The hypothetical reaction model now locates splitting in both reactions prior to formation of a covalent intermediate during the catalytic cycle.

Dipeptidyl Peptidase 4↗
PubMed1997

Kinetic study of irreversible inhibition of an enzyme consumed in the reaction it catalyses. Application to the inhibition of the puromycin reaction by spiramycin and hydroxylamine.

A systematic procedure for the kinetic study of irreversible inhibition when the enzyme is consumed in the reaction which it catalyses, has been developed and analysed. Whereas in most reactions the enzymes are regenerated after each catalytic event and serve as reusable transacting effectors, in the consumed enzymes each catalytic center participates only once and there is no enzyme turnover. A systematic kinetic analysis of irreversible inhibition of these enzyme reactions is presented. Based on the algebraic criteria proposed in this work, it should be possible to evaluate either the mechanism of inhibition (complexing or non-complexing), or the type of inhibition (competitive, non-competitive, uncompetitive, mixed non-competitive). In addition, all kinetic constants involved in each case could be calculated. An experimental application of this analysis is also presented, concerning peptide bond formation in vitro. Using the puromycin reaction, which is a model reaction for the study of peptide bond formation in vitro and which follows the same kinetic law as the enzymes under study, we have found that: (i) the antibiotic spiramycin inhibits the puromycin reaction as a competitive irreversible inhibitor in a one step mechanism with an association rate constant equal to 1.3 x 10(4) M-1 s-1 and, (ii) hydroxylamine inhibits the same reaction as an irreversible non-competitive inhibitor also in a one step mechanism with a rate constant equal to 1.6 x 10(-3) M-1 s-1.

Acyltransferases↗
PubMedDate not supplied

Synthesis of the O-(2,3,4,5,6-pentafluorobenzyl)hydroxylamine oximes of selected carbonyl compounds and their determination by liquid chromatography with ultraviolet detection.

The aims were to develop a liquid chromatographic (LC) method with ultraviolet detection (UVD) for O-(2,3,4,5,6-pentafluorobenzyl)hydroxylamine hydrochloride (PFBHA) O-oximes of common aldehydes and ketones, and to define the steric limits of the synthetic reaction used to make the PFBHA O-oxime standards for gas chromatographic (GC) and LC methods. Ten new O-oximes were synthesized with the new optimized method, and their purities were demonstrated by GC/electron-capture detection (ECD), GC/mass spectrometry (MS), ultraviolet spectroscopy, infrared spectroscopy, and proton and 13C-nuclear magnetic resonance spectroscopy. Ketones substituted at both beta-carbons relative to the carbonyl carbon, like diisobutyl ketone and 2,4-hexanedione, showed lower synthetic yields by wet chemistry methods. A new C18 reverse-phase LC method with UVD at 200 nm and acetonitrile-water in both the isocratic and gradient-elution modes was then developed to sensitively resolve a mixture of 13 pure PFBHA O-oximes. The detection limit was near 100 ng O-oxime/mL or about 14-50 ng aldehyde/mL and the least quantifiable limits were near 500 ng/mL or about 70-250 ng aldehyde/mL, with lower limits for glyoxal, methylglyoxal, benzaldehyde, and acetophenone. Carbonyl compounds in 500 mL water samples were then determined in distilled water and tap water by gradient elution. Vapors of n-valeraldehyde and acrolein generated in gas bags at concentrations near occupational guidelines were also sampled, desorbed, and then determined by either isocratic or gradient elution at 200 or 254 nm within 30-45 min.

Chromatography, Liquid↗
PubMed2004

Effects of hydroxylamine on microbial community structure and function of autotrophic nitrifying biofilms determined by in situ hybridization and the use of microelectrodes.

Effects of hydroxylamine (NH2OH), an intermediate of NH4+ oxidation, on microbial community structure and function of two autotrophic nitrifying biofilms fed with and without NH2OH were analyzed by a 16S rRNA approach and the use of microelectrodes. In the NH2OH-added biofilm, partial oxidation of NH4+ to NO2- was observed, whereas complete oxidation of NH4+ to NO3- was achieved in the control biofilm. In situ hybridization results revealed that no nitrite-oxidizing bacteria (NOB) hybridized with any specific probes were detected in the NH2OH-added biofilm. Thus, the addition of low concentrations of NH2OH (250 microM) completely inhibited the growth of NOB. Phylogenetic analysis of 16S rDNA indicated that the ammonia-oxidizing bacteria (AOB) detected in both biofilms were closely related to Nitrosomonas europaea, and that the clone sequences from both biofilm libraries have more than 99% similarity to each other. However, in situ hybridization results revealed that the addition of NH2OH changed the form of growth pattern of the dominant Nitrosomonas spp. from dense clusters mode to single scattered cells mode. Microelectrode measurements revealed that the average NH4+ consumption rate calculated in the NH2OH-added biofilm was two times higher than that in the control biofilm. This clearly demonstrated that the oxidation of NH4+ was stimulated by NH2OH addition.

Biofilms↗
PubMed1986

Aminations of guanosine and deoxyguanosine with hydroxylamine-O-sulfonic acid and 2,4-dinitrophenoxyamine. Dependence on the reaction medium.

Amination of guanosine (Guo) with 2,4-dinitrophenoxyamine in aqueous DMF gave 7-amino-Guo, which was readily converted to 8,5'-O-cyclo-Guo, and 8-hydroxy-Guo. Deoxyguanosine (dG) gave only deglycosylated 7-amino-G under the same reaction condition. Aminations of Guo and dG with hydroxylamine-O-sulfonic acid above pH 9 gave the corresponding 1-amino derivatives, whereas those in acidic media at pH 2-4 gave 8-amino-Guo and 7-amino-G as the main products, respectively. Amination of Guo in neutral media gave 1-amino-Guo and decomposed products of 7-amino-Guo. The mechanisms of these amination reactions are described.

Deoxyguanosine↗
PubMed1977

Selective formation of certain amino acids from formaldehyde and hydroxylamine in a modified sea medium enriched with molybdate.

Amino acids produced from formaldehyde and hydroxylamine in modified sea mediums with different concentrations of molybdate were analyzed. The modified sea mediums contained lower concentration of sodium chloride and higher concentrations of transition metal ions (Zn2+, Fe3+, Cu2+, Co2+, Mn2+ each 10(-4)m, and Mo O4(2-)10(-6), 10(-4), or 10(-2)m) than sea water. The concentration of molybdate had apparently no remarkable effect on the total yields of primary amino groups, but a remarkable effect on the nature of amino acids produced. The formation of alanine, aspartic acid, beta-alanine and, in particular, proline was increased, and that of glycine and serine was decreased with the enrichment of molybdate. The results suggest the possibility of a natural selection of prebiotic organic molecules based on the nature of environmental catalysers in the course of chemical evolution.

Amino Acids↗
PubMedDate not supplied

Cytochrome P-455-nm complex formation in the metabolism of phenylalkylamines. VI. Structure--activity relationships in metabolic intermediary complex formation with a series of alpha-substituted 2-phenylethylamines and corresponding N-hydroxylamines.

The formation of cytochrome P-450 metabolic intermediary (MI) complexes from a homologous series of alpha-substituted 2-phenylethylamines and corresponding N-hydroxylamines was investigated during NADPH-dependent metabolism in liver microsomes from phenobarbital-pretreated rats. The alpha-alkyl substituent consisted of branched and unbranched alkyl chains ranging from 0-4 carbons and the benzyl group. All the compounds but 2-phenylethylamine generated the complex and double-reciprocal plots of the highest observed rate of complex formation vs. substrate concentration gave linear relations over a defined substrate range. The Vmax(obs) values for complex formation by the amines increased markedly with increasing size of the alkyl group and a good correlation was obtained between log Vmax(obs) and the logarithm of the octanol/buffer partition coefficient of the substrates. With the N-hydroxy compounds, complex formation was a much less selective phenomenon and without exception the rates were quite high with Vmax(obs) values as much as 100 times greater than those of the amines. The disappearance of substrate amines was independent of structure and at an initial substrate concentration of 100 microM about a 50% decrease was noted during a 20-min period in all cases. The results substantiate the previous notion that N-oxidation is a prerequisite for MI-complex formation from primary amines. The results also suggest that C- and N-oxidation have different rate-limiting steps and the microsomal enzymes catalyzing the N-oxidation seem to be deeply submerged in the lipid matrix, as amines with a low distribution are inactive or poor substrates for generating the cytochrome P-450 ligand. Also, it is evident that the MI complex formation does not impair the overall metabolism of the amines.

Animals↗
PubMed1983

Cyanide prevents the inhibition of platelet aggregation by nitroprusside, hydroxylamine and azide.

Sodium cyanide (CN-) in concentrations of 10 uM or more prevented the inhibition of epinephrine (2.5 uM) and of ADP (4.0 uM) induced primary and secondary aggregation brought about by 10 uM sodium nitroprusside (SNP). Cyanide alone in the same concentration had no effect on platelet aggregation induced by epinephrine or ADP. Even when the addition of CN- was delayed for as long as 9 min after epinephrine and SNP, it immediately reversed the SNP block and initiated a bimodal wave of aggregation. The effect of CN- on SNP inhibition of platelet aggregation appears to be competitive and reversible. Although they are less potent inhibitors of platelet aggregation than SNP, the effects of hydroxylamine (HA) and azide were also prevented by SNP. In our hands, sodium nitrite did not inhibit platelet aggregation consistently. The inhibitory effects of glyceryl trinitrate, papaverine and nitric oxide hemoglobin on platelet aggregation were not prevented by CN-. These interactions probably have no significance in vivo, but they indicate that SNP, HA and azide act on platelets and on vascular smooth muscle by similar or identical biochemical mechanisms. They also suggest that there are at least two sub-classes of so-called nitric oxide vasodilators. The effect of CN- may be mediated through an inhibition of the formation of nitric oxide from SNP, HA and azide.

Azides↗
PubMed1984

Hydroxylamine and methoxyamine mutagenesis: tautomeric equilibrium of the promutagenic, N6-methoxyadenosine in solvents of different polarities.

Ultraviolet (UV) and Infrared (IR) spectroscopy have been applied to a study of the tautomeric equilibrium, in solvents of varying polarities and differing hydrogen bond donor-acceptor properties, of the promutagenic analogue N6- methoxyadenosine , the product of the reaction of the mutagen methoxyamine with adenosine. In the non-polar solvent CCl4, the analogue is predominantly in the amino form, with KT approximately 10. On transfer from CCl4 to chloroform, dimethyl sulfoxide, and water, the equilibrium is shifted stepwise towards the imino form, attaining a KT approximately 10 in favour of the imino species in aqueous medium. Both the UV and, particularly, the IR spectra exhibit two sets of absorption bands which were assigned to the respective tautomers , in dynamic equilibrium with each other. The significance of the foregoing results in the mechanism of hydroxylamine (and methoxyamine) mutagenesis is considered. It is also shown that base pairing of each tautomeric species is significantly dependent on the conformation of the exocyclic N6-methoxy group. It is further demonstrated that infrared spectroscopy provides data which both supplement and extend those obtained by NMR spectroscopy, under conditions where application of the latter is technically limited.

Adenosine↗
PubMed1975

[The influence of adenine, adenosine and adenylic nucleotides on the mutagenic action of hydroxylamine].

The effect of some adenyl precurosors of DNA synthesis on the mutagenic activity oh hydroxylamine (HA) is studied. It is shown that the addition of adenine to a suspension of Escherichia coli Bcells increases the yield of mutants by more than two times as compared with HA alone. The effects of adenosine, AMP and dAMP are somewhat different. It is suggested that the increase of the HAmutagenic effect produced by the addition of adenine may be due to:1) the excess of the amount of adenylic precursors of DNA synthesis over guanilic ones, which promotes the erroneous base-pairing during the replication of the HA modified template; 2) the modification of adenylic precursors by HA into N6-oxy-dATP, and their incorporation into DNA. The mutagenic effect of N6-hydroxyadenosine, the product of the adenine modification by HA, in E. coli Bpur- was studied. The experiments showed that N6-hydroxyadenosine induced about 1% of mutations, a relatively low lethal effect (the cell survival was 80%), and provided a high mutagenic action of this compound.

Adenine↗
PubMed1975

[Effect of adenine, adenosine and adenylic nucleotides on the mutagenic action of hydroxylamine].

The effect of some adenyl precursors of DNA synthesis on the mutagenic activity of hydroxylamine (HA) is studied. It is shown that the addition of adenine to a suspension of Escherichia coli B cells increases the yield of mutants by more than two times as compared with HA alone. The effects of adenosine, AMP and dAMP are somewhat different. It is suggested that the increase of the HA mutagenic effect produced by the addition of adenine may be due to: 1) the excess of the amount of adenylic precursors of DNA synthesis over guanilic ones, which promotes the erroneous base-pairing during the replication of the HA modified template; 2) the modification of adenylic precursors by HA into N6-oxy-dATP, and their incorporation into DNA. The mutagenic effect of N6-hydroxyadenosine, the product of the adenine modification by HA, in E. coli B pur- was studied. The experiments showed that N6-hyrdoxyadenosine induced about 1% of mutations, a relatively low lethal effect (the cell survival was 80%), and provided a high mutagenic action of this compound.

Adenine↗
PubMed1975

[Effect of adenine, adenosine and adenylic nucleotides on the mutagenic effect of hydroxylamine].

The effect of some adenyl precursors of DNA synthesis on the mutagenic activity of hydroxylamine (HA) is studied. It is shown that the addition of adenine to a suspension of Escherichia coli B cells increases the yield of mutants by more than two times as compared with HA alone. The effects of adenosine, AMP and dAMP are somewhat different. It is suggested that the increase of the HA mutagenic effect produced by the addition of adenine may be due to: 1) the excess of the amount of adenylic precursors of DNA synthesis over guanilic ones, which promotes the erroneous base-pairing during the replication of the HA modified template; 2) the modification of adenylic precursors by HA into N6-oxy-dATP, and their incorporation into DNA. The mutagenic effect of N6-hydroxyadenosine, the product of the adenine modification by HA, in E. coli B pur- was studied. The experiments showed that N6-hydroxyadenosine induced about 1% of mutations, a relatively low lethal effect (the cell survival was 80%), and provided a high mutagenic action of this compound.

Adenine↗
PubMed1990

Electrophoresis at elevated hydrostatic pressure of the multiheme hydroxylamine oxidoreductase.

The behavior of the multiheme protein hydroxylamine oxidoreductase (HAO) in polyacrylamide gel electrophoresis was studied at hydrostatic pressures up to 3 kbar at 25 degrees C. Due to the limited working volume of the high pressure vessel, the electrophoresis cells were miniaturized. A microcell which accommodates 6 capillary gel tubes is described. Between 1 bar and 1.5 kbar the enzyme did not undergo structural changes detectable in the gel system. At approximately 2 kbar the active form of the enzyme was partially dissociated. At higher pressures, the enzyme was converted to forms which were irreversibly inactive and had a higher apparent molecular mass, suggesting aggregation or denaturation.

Atmospheric Pressure↗
PubMed1993

In vitro embryotoxicity of N-methyl-N-(7-propoxynaphthalene-2-ethyl)hydroxylamine (QAB): evidence for N-dehydroxylated metabolite as a proximate dysmorphogen.

The rat conceptus biotransforms N-methyl-N-(7-propoxynaphthalene-2-ethyl)hydroxylamine (QAB) in vitro to 7-propoxynaphthalen-2-ylacetic acid (QAA) and six more (M1 to M6) metabolites. Thus far, M4 has been identified as N-demethyl-QAB and M6 as N-desoxy-QAB. We investigated which of these two metabolites might be involved in QAB-embryotoxicity in vitro. Conceptuses were cultured from day 9.5 to 11.5 post-coitum, and were exposed to N-demethyl-QAB or N-desoxy-QAB either in the culture medium or by microinjection directly into the amniotic cavity. When added to the culture medium, N-demethyl-QAB (No Observed Adverse Effect Level, NOAEL, for growth 122 microM and for differentiation 41 microM) was less active than QAB itself (NOAEL for growth and differentiation 12 microM). N-desoxy-QAB caused severe growth retardation and an impairment of differentiation at a concentration of 11 microM (NOAEL 3.6 microM). As regards causing anomalies, the NOAEL of N-demethyl-QAB (41 microM) was 10-fold higher than that of QAB (NOAEL 3.9 microM) and that of N-desoxy-QAB (NOAEL 3.6 microM). At an intraamniotic concentration of 0.7 mM, N-demethyl-QAB caused no effects on growth and differentiation and no increase of anomalies was observed, whereas QAB and N-desoxy-QAB each elicited an increase in dysmorphogenic embryos at equimolar concentrations without affecting growth and differentiation. It is, therefore, concluded that N-desoxy-QAB, but not N-demethyl-QAB, could be a proximate dysmorphogen responsible for the embryotoxicity/teratogenicity of QAB in vitro.

Abnormalities, Drug-Induced↗