Disease relevance of N-hydroxyethanamide

• A randomized double-blind study of acetohydroxamic acid in struvite nephrolithiasis [1].
• Episodes of tremulousness (n = 5, P less than 0.05), which reversed with a decrease in drug dose, and phlebothrombosis (n = 3, P not significant) were limited to the group given acetohydroxamic acid [1].
• Eighteen patients who received acetohydroxamic acid (15 mg per kilogram of body weight per day, in divided oral doses) for a mean of 15.8 months were compared in a randomized double-blind study with 19 patients who received placebo for a mean of 19.6 months [1].
• We conclude that acetohydroxamic acid effectively inhibits the growth of struvite stones in the short term in patients infected with urea-splitting bacteria, but the prevalence of adverse reactions appears to be high and the toxicity and effectiveness of long-term therapy for struvite nephrolithiasis remain to be defined [1].
• Inhibition of Helicobacter pylori by acetohydroxamic acid [2].

High impact information on N-hydroxyethanamide

• In this study of the exchange of Fe3+ between acetohydroxamic acid and transferrin such evidence has been found [3].
• Ten days after acetohydroxamic acid, the urea breath test values were similar to those before treatment [4].
• Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects [4].
• Inhibition of Jack Bean urease (EC 3.5.1.5) by acetohydroxamic acid and by phosphoramidate. An equivalent weight for urease [5].
• Hypercoagulability produced by treatment with acetohydroxamic acid [6].

Chemical compound and disease context of N-hydroxyethanamide

• Helicobacter pylori exhibits chemotactic responses to urea, flurofamide, acetohydroxamic acid, and sodium bicarbonate [7].
• In the present context, phosphatidyl ethanolamine (PE) liposomes anchored polyvinyl alcohol (PVA) xerogel beads (lipobeads) bearing acetohydroxamic acid (AHA) was developed as a receptor-mediated drug delivery system for use in blocking adhesion of Helicobacter pylori and thereby preventing the sequelae of chronic gastric infections [8].
• Calcite precipitation induced by both B. pasteurii and E. coli (pBU11) was inhibited in the presence of a urease inhibitor, acetohydroxamic acid (AHA) [9].
• Whereas similar results were found for GM 1489, an analog of GM 6001, acetohydroxamic acid, containing the critical metal ligand group but without the amino acid side chains necessary for binding to the MMPs, did not alter the response to PdiBu inflammation/hyperplasia [10].

Biological context of N-hydroxyethanamide

• However, the addition of acetohydroxamic acid (200 mg/liter), a potent urease inhibitor which inhibits ammonia production, did not completely restore cell growth, suggesting the difficulty of neutralizing the ammonia in the vicinity of the cells [11].
• Viabilities of cells exposed to H. pylori for 2, 24, and 48 h, assessed by incorporation of neutral red dye, were 60, 27, and 16%, respectively; however, the viabilities of cells exposed to both H. pylori and acetohydroxamic acid were 92, 46, and 20% after 2, 24, and 48 h, respectively, (P less than 0.001) [12].
• The effect of antibiotics and acetohydroxamic acid on bacterial hydrolysis of urea [13].
• Adjustment of the parameters used by DOCK, in order to account for the presence of the metal ion in the active site, resulted in the calculation of best energy structures for the nickel-bound inhibitors beta-mercaptoethanol, acetohydroxamic acid, and diamidophosphoric acid [14].
• Kinetics and mechanism of iron(III)-nitrilotriacetate complex reactions with phosphate and acetohydroxamic acid [15].

Anatomical context of N-hydroxyethanamide

• Gastric cells cultured in medium supplemented with 20 mM urea were exposed to 5 x 10(6) CFU of H. pylori per ml with or without the addition of a urease inhibitor, acetohydroxamic acid [12].
• Easily achievable concentrations of acetohydroxamic acid in vitro systems that simulated the dynamics of the urinary tract potentiated the antibacterial effect of methenamine against Proteus species [16].
• A randomized trial of acetohydroxamic acid for the treatment and prevention of infection-induced urinary stones in spinal cord injury patients [17].
• The observation that both hydroxyurea and the structurally related compounds acetohydroxamic acid and N-hydroxyurethane induce DNA repair in primary hepatocyte cultures suggests that metabolism-dependent genotoxicity may be a common property of aliphatic hydroxamic acids [18].
• In an effort to augment the anti-H. pylori effect of acetohydroxamic acid (AHA), floating PC microspheres, which have the ability to reside in the gastrointestinal (GI) tract for an extended period, were prepared by emulsion (O/W) solvent evaporation technique [19].

Associations of N-hydroxyethanamide with other chemical compounds

• The enzyme was cytoplasmic in P. stuartii, was inhibited in vitro by hydroxyurea, acetohydroxamic acid, and EDTA, and appears to have a complex subunit structure and a unique molecular size within genera of the Proteeae tribe [20].
• Treatment of a new chelate ligand having both amide- and phenyl-appended pyridyl moieties with Ni(ClO4).6H2O and acetohydroxamic acid in methanol solution results in the production of a novel pseudo-octahedral Ni(II) complex having a neutral acetohydroxamic acid ligand stabilized by a hydrogen-bonding interaction [21].
• 7. Neither bilateral vagotomy, nor selective inhibition of arachidonate cyclo-oxygenase with indomethacin or 5-lipoxygenase with the novel acetohydroxamic acid BW A4C, significantly reduced the bronchoconstrictor effect of inhaled PGD2.(ABSTRACT TRUNCATED AT 250 WORDS)[22]
• The kinetics and mechanism of the substitution of coordinated water in nitrilotriacetate complexes of iron(III) (Fe(NTA)(OH(2))(2) and Fe(NTA)(OH(2))(OH)(-)) by phosphate (H(2)PO(4)(-) and HPO(4)(2)(-)) and acetohydroxamic acid (CH(3)C(O)N(OH)H) were investigated [15].
• Using the X-ray absorption spectroscopy (XAS) at the Fe- and N-K absorption edges, we characterized the nature of Fe(III) interactions with a hydroxamate siderophore, desferrioxamine B (desB), and its small structural analogue, acetohydroxamic acid (aHa), as a function of pH (1.4-11.4) [23].

Gene context of N-hydroxyethanamide

• AHA and/or BOC-MLP decreased IL-8 production at 2-4 h after stimulation [24].
• These results, taken together with the X-ray structure of the adduct between MMP-12, the inhibitor 20 and the acetohydroxamic acid (AHA), suggest that bicyclic scaffold derivatives may be exploited for the design of new selective matrix metalloproteinase inhibitors (MMPIs) [25].
• Acetohydroxamic acid blocked the NRU induced by jack bean urease and urea but failed to block the uptake induced by H. pylori supernatants [26].
• After acetohydroxamic acid (AHA) and/or N-tert-butoxycarbonyl-methionyl-leucyl-phenylalanine (BOC-MLP) was added to H. pylori culture supernatant, IL-8 ELISA was analyzed for 9 h [24].

Analytical, diagnostic and therapeutic context of N-hydroxyethanamide

• Long-term chemotherapy with antimicrobial agents that achieve steril urine or acetohydroxamic acid in those patients with recalcitrant infection lessens the risk of recurrent calculogenesis [27].
• In both recombinant and cell culture assays, the new ZBGs were found to be effective inhibitors, typically 10-100-fold more potent than acetohydroxamic acid [28].
• The alkalinization and crystallization caused by Ureaplasma urealyticum and Proteus mirabilis was completely prevented by acetohydroxamic acid, a potent urease inhibitor, linking the crystallization to the urease activity of the microorganisms [29].
• Acetohydroxamic acid, an inhibitor of the bacterial urease enzyme, is currently undergoing clinical trials to determine whether or not it can prevent stone growth in patients at risk [30].
• Only membrane-bound activity was inhibited with AHA but not the activity localized within the cytoplasma as demonstrated by electron-microscopy [31].

References