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Chemical Compound Review

CID5288043     N'-[5-(ethanoyl-hydroxy- amino)pentyl]-N...

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Disease relevance of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide


Psychiatry related information on N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide


High impact information on N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide

  • When Desferal, an iron chelator, was added to these combinations, the four-drug combinations increased inhibition of cell growth and increased cytotoxicity [7].
  • To prevent enzyme inhibition, erythrocyte membranes were treated with tBHP in the presence of 1 mmol/L ascorbate, a potential antioxidant, and 1 mmol/L desferal, an iron chelator [8].
  • The antioxidant, desferal, also diminished increased mitochondrial Ca2+ after t-BuOOH and prevented cell death [9].
  • H2O2-induced expression was prevented by catalase but unaffected by Desferal, indicating that metal catalyzed degradation of peroxide was not involved [10].
  • From reported results we conclude that BPYTA is a powerful RR inhibitor (R2 subunit) which has a different mechanism of action from that of Desferal [11].

Chemical compound and disease context of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide


Biological context of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide

  • Desferal and hemin modulated iron-responsive element binding activity in HL-60 cells without affecting the phosphorylation state of IRP1 [15].
  • The iron chelator desferal and the intracellular spin trap PBN caused a significant reduction in oxidative stress to almost control levels [16].
  • The hydroxylation of salicylate was attenuated in mice treated with desferal while there was no effect of l-NAME compared with untreated mice [17].
  • Three of the selected chelators (M30, HLA20 and M32) were the most effective in inhibiting iron-dependent lipid peroxidation in rat brain homogenates with IC50 values (12-16 microM), which is comparable with that of desferal, a prototype iron chelator that is not has orally active [18].
  • The virulence of YeO3-R2 was determined in an orally infected desferal-attenuated murine model [19].

Anatomical context of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide

  • In HL-60 cells, hemin (an iron source) stimulated m-Acon synthesis 3-fold after 4 h compared with cells treated with an iron chelator (Desferal) [20].
  • In contrast to its effect on tumor cells, desferal did not inhibit growth of normal breast epithelial cells [2].
  • Desferal (desferrioxamine)--a novel activator of connective tissue-type mast cells [21].
  • Furthermore, the modulation of "basal" or "UVA-induced" level of LIP by either Desferal and/or hemin treatment significantly affected the extent of UVA-induced necrotic cell death and ATP depletion in all the cell lines [22].
  • One- and two-electron reduction of quinone I led to calf thymus DNA-strand-break formation, a process that (a) was substantially decreased in experiments performed with dialysed DNA and in the presence of desferal and (b) was partially sensitive to superoxide dismutase and/or catalase [23].

Associations of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide with other chemical compounds

  • The effect of Desferal (desferrioxamine), an iron-chelating agent with allergic side effects, was examined on human basophils and rodent mast cells (MCs) in vitro and in the human skin [21].
  • Reversed siderophores as antimalarial agents. II. Selective scavenging of Fe(III) from parasitized erythrocytes by a fluorescent derivative of desferal [24].
  • Finally, we summarize the effects of cerebroprotective pharmacological agents including the iron chelator desferal, superoxide dismutase, a stable radical from the nitroxide family, and HU-211, a nonpsychotoropic cannabinoid with antioxidant properties [25].
  • In order to test the hypothesis that decreasing the vascular level of iron slows lesion growth, we examined the effects of the iron chelator Desferal (72 mg/kg/day, 5 days/week) on atherosclerosis and lesion iron content in cholesterol-fed New Zealand White rabbits [26].
  • Treatment of intact liver and liver homogenate with sodium nitrite, or desferal, brings about the appearance of g = 2.03 and g = 4.3 electron paramagnetic resonance spectroscopy (EPR) signals, respectively [27].

Gene context of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide

  • The cytostatic activity of desferal was partially ameliorated by pretreatment with iron-saturated transferrin, and transferrin receptor expression on breast cancer cells nearly doubled after exposure to desferal [2].
  • The effects of adding iron, transferrin, or Desferal (an iron chelate) upon the growth of V. vulnificus in human and rabbit sera were also examined [28].
  • The fact that the four-line spectrum obtained for the Abeta/PBN in PBS was completely abolished in the presence of the iron-chelating agent Desferal demonstrated the observed four-line spectrum to be iron-dependent [29].
  • Further treatment with PIH or desferrioxamine (Desferal) increased the synthesis of TfR mRNA in induced Friend cells [30].
  • Immuno-modulation of human lymphocyte function by desferroxamine (Desferal) [31].

Analytical, diagnostic and therapeutic context of N'-[5-(acetyl-hydroxy-amino)pentyl]-N-hydroxy-N-[5-[3-(hydroxy-methyl-carbamoyl)propanoylamino]pentyl]butanediamide

  • In contrast, in all seven subjects studied, intradermal injection of Desferal (0.1 mg/ml to 100 mg/ml) elicited classic wheal-and-flare responses [21].
  • Iron restriction caused a significant reduction in infectivity of C. trachomatis elementary bodies (EB) harvested from Desferal-exposed polarized epithelial cells when compared to that of EB harvested from iron-sufficient control cell cultures [12].
  • Desferrithiocin stimulates ferritin iron mobilization, when administered either by gavage or by intraperitoneal injection, whereas desferal is active intraperitoneally but inactive orally [13].
  • Using fast cyclic voltammetry, tyrosine hydroxylase (TH) immunohistochemistry, Perls' iron staining, and high-performance liquid chromatography-electrochemical detection, we measured the degeneration of dopaminergic neurons and increased iron content in the SN of rats overloaded with iron dextran and assessed the effects of treatment with Desferal [32].
  • Pretreatment with dimethylthiourea (DMTU) or addition of desferal to the perfusate also significantly reduced the protein oxidation of lung ischemia/reperfusion [33].


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  8. Increased susceptibility of the sickle cell membrane Ca2+ + Mg(2+)-ATPase to t-butylhydroperoxide: protective effects of ascorbate and desferal. Moore, R.B., Hulgan, T.M., Green, J.W., Jenkins, L.D. Blood (1992) [Pubmed]
  9. Contribution of increased mitochondrial free Ca2+ to the mitochondrial permeability transition induced by tert-butylhydroperoxide in rat hepatocytes. Byrne, A.M., Lemasters, J.J., Nieminen, A.L. Hepatology (1999) [Pubmed]
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  11. 2,2'-Bipyridyl-6-carbothioamide and its ferrous complex: their in vitro antitumoral activity related to the inhibition of ribonucleotide reductase R2 subunit. Nocentini, G., Federici, F., Franchetti, P., Barzi, A. Cancer Res. (1993) [Pubmed]
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  17. Microdialysis studies of extracellular reactive oxygen species in skeletal muscle: factors influencing the reduction of cytochrome c and hydroxylation of salicylate. Close, G.L., Ashton, T., McArdle, A., Jackson, M.J. Free Radic. Biol. Med. (2005) [Pubmed]
  18. Novel multifunctional neuroprotective iron chelator-monoamine oxidase inhibitor drugs for neurodegenerative diseases: in vitro studies on antioxidant activity, prevention of lipid peroxide formation and monoamine oxidase inhibition. Zheng, H., Gal, S., Weiner, L.M., Bar-Am, O., Warshawsky, A., Fridkin, M., Youdim, M.B. J. Neurochem. (2005) [Pubmed]
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  22. Susceptibility of skin cells to UVA-induced necrotic cell death reflects the intracellular level of labile iron. Zhong, J.L., Yiakouvaki, A., Holley, P., Tyrrell, R.M., Pourzand, C. J. Invest. Dermatol. (2004) [Pubmed]
  23. One- and two-electron reduction of 2-methyl-1,4-naphthoquinone bioreductive alkylating agents: kinetic studies, free-radical production, thiol oxidation and DNA-strand-break formation. Giulivi, C., Cadenas, E. Biochem. J. (1994) [Pubmed]
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