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Chemical Compound Review

Ferlucon     iron; (2R,3R,4S,5S)-2,3,4,5,6...

Synonyms: Flourish, Glucomax, Cerevon, Feravol, Ferrose, ...
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Disease relevance of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • An in vitro Fenton system was established that generates DNA strand breaks and inactivates bacteriophage and that also reproduces the suppression of DNA damage by high concentrations of peroxide [1].
  • Little is known about changes in the amount of iron in the intracellular low molecular weight pool, which catalyzes the Fenton reactions during reperfusion after ischemia [2].
  • Inhaled silicate dusts may cause lung disease through their surface coordination of iron with subsequent oxidant generation via the Fenton reaction [3].
  • A major portion of H2O2 toxicity is attributed to DNA damage caused by the iron-mediated Fenton reaction [4].
  • These observations confirm unique renoprotective properties of ARB, independent of BP lowering but related to decreased oxidative stress (hydroxyl radicals scavenging and inhibition of the Fenton reaction), correction of chronic hypoxia, and inhibition of advanced glycation end product formation and of abnormal iron deposition [5].

Psychiatry related information on (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • Free radicals in disease pathogenesis, generated in part as a result of Fenton-type reactions, suggest that lowering the level of available iron, intervention with antioxidants, or the administration of free radical scavengers could provide a therapeutic inroad in the fight against Alzheimer's disease [6].
  • The optimal reaction times in the Fenton and Photo-Fenton processes were 60 min and 80 min, respectively [7].

High impact information on (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro [1].
  • Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents [8].
  • These findings suggest that asbestos inhalation can induce inducible nitric oxide synthase activation and peroxynitrite formation in vivo, and provide evidence of a possible alternative mechanism of asbestos-induced injury to that thought to be induced by Fenton reactions [9].
  • The reactivity of H2O2 with iron (Fenton reaction) intimately connects oxidative stress and cellular iron metabolism [10].
  • Thus, the localized Fenton reaction appears to impact the expression of hypoxia-regulated genes by means of HIF-1alpha stabilization and coactivator recruitment [11].

Chemical compound and disease context of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid


Biological context of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • By studying DNA damage during Fenton reactions in vitro, the same complex kinetics were observed and three types of oxidants were distinguished based upon their reactivities toward H2O2 and alcohols and upon iron-chelator effects [4].
  • Thus, it was the aim of this study to localize the cellular compartment in which the Fenton reaction takes place and to determine whether scavenging of.OH can modulate hypoxia-inducible factor 1 (HIF-1)-dependent gene expression [11].
  • The amino acid sequence of the rat ornithine carbamoyltransferase was compared with the recently reported sequence of the human enzyme [Horwich, A. L., Fenton, W. A., Williams, K. R., Kalousek, F., Kraus, J. P., Doolittle, R. F., Konigsberg, W. & Rosenberg, L. E. (1984) Science 224, 1068-1074] [17].
  • Our previous characterization of the IL1B promoter indicated that the region between -131 and +12 is sufficient to direct cell-type-specific expression of a reporter gene (F. Shirakawa, K. Saito, C.A. Bonagura, D.L. Galson, M.J. Fenton, A.C. Webb, and P. E. Auron, Mol. Cell. Biol. 13:1332-1344, 1993) [18].
  • These adducts are formed from lipid peroxidation products (F. El-Ghissassi et al., Chem. Res. Toxicol., 8: 273-283, 1995) and thus could arise in the liver of LEC rats from oxygen radicals generated by copper-catalyzed Fenton-type reactions [19].

Anatomical context of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • A Fenton reaction at the endoplasmic reticulum is involved in the redox control of hypoxia-inducible gene expression [11].
  • During exposure to peroxide only, the iron in sickle membranes was unable to act as a Fenton catalyst without addition of a reducing agent [20].
  • However, when we measured the Fenton chemistry educt hydrogen peroxide and its precursor, the superoxide anion radical, formation of both had markedly decreased and steady-state levels of hydrogen peroxide did not alter during cold incubation of either liver endothelial cells or hepatocytes [21].
  • The results of this study demonstrated that the protection provided by DFO and other HAs against TCHQ-induced cyto- and genotoxicity in human fibroblasts is mainly through scavenging of the observed reactive TCSQ radical and not through prevention of the Fenton reaction by the binding of iron in a redox-inactive form [22].
  • Fenton-like reactions may be commonly associated with most membranous fractions including mitochondria, microsomes, and peroxisomes [23].

Associations of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid with other chemical compounds

  • In this study, we investigated whether iron, a potent source of the highly reactive hydroxyl radical that is generated by the Fenton reaction with H2O2, might contribute to the source of radicals in Alzheimer disease [24].
  • In vitro and in vivo analyses showed that H(2)O(2) directly oxidized their solvent-exposed clusters in a Fenton-like reaction [25].
  • Separate determinations of the two redox half-reactions involved (i.e. Fe3+ + O-.2----Fe2+ + O2 and Fe2+ + H2O2----Fe3+ + .OH + OH-) indicate that an available coordination site is necessary for the latter (Fenton) reaction [26].
  • H2O2 alone decreases the viscosity of HA, presumably by the Fenton reaction, in the absence (but not in the presence) of the iron chelator, diethyltriaminepentacetic acid (DETAPAC) [27].
  • To develop a method for estimating total HO. production, we studied two model systems: the superoxide driven Fenton reaction in vitro, using xanthine oxidase as the source of superoxide, and a computer model of Fenton chemistry [28].

Gene context of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • ESR spin-trapping studies demonstrated that GIF at 2-6 microm scavenged hydroxyl radicals generated by a Fenton-type reaction or the photolysis of hydrogen peroxide much more effectively than the same concentration of metallothionein I+II [29].
  • Consistent with the damage specificity above, hSMUG1 removed damaged bases from Fenton-oxidized calf thymus DNA, generating abasic sites [30].
  • The aconitase-released Fe(2+) combines with H(2)O(2) to generate *OH via a Fenton reaction and the oxidized Fe(3+) recombines with the inactivated enzyme after being reduced to Fe(2+) by other cellular reductants, turning it over to be active [31].
  • These results suggest that PrPC modulates the intracellular H2O2 level as a copper-binding protein to protect CGNs from apoptotic cell death possibly due to inhibiting a Fenton reaction [32].
  • Mechanisms of Saccharomyces cerevisiae PMA1 H+-ATPase inactivation by Fe2+, H2O2 and Fenton reagents [33].

Analytical, diagnostic and therapeutic context of (2R,3R,4S,5S)-2,3,4,5,6-pentahydroxyhexanoic acid

  • The Fenton reaction could be localized in a perinuclear space by confocal laser microscopy and three-dimensional reconstruction techniques [34].
  • CONCLUSIONS: The use of Fenton-like chemistry in SPIE-IA technology allows a sensitive measurement of E2 in human serum and could be a new approach for the development of sensitive immunoassays [35].
  • The production of *OH in the supernatant of cultured rabbit corneal fibroblasts by the Fenton reaction caused an increase in PI (+) and TUNEL (+) cells by 90 minutes, which was significantly inhibited by the addition of DMSO [36].
  • Similar Fenton-type treatment of the purine dinucleotides dApdG and dApdA resulted in products that were chromatographically identical on anion-exchange TLC and on reverse-phase HPLC to the two major products generated in DNA [37].
  • Similar treatment of the double-stranded plasmid pBluescript K+ with hydrogen peroxide (1 mM) and each transition-metal ion (1-100 microM) followed by quantitative agarose gel electrophoresis demonstrated that open-circle DNA, resulting from single-strand breaks, was generated in Fenton reactions involving all nine metal ions [38].


  1. Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro. Imlay, J.A., Chin, S.M., Linn, S. Science (1988) [Pubmed]
  2. Low molecular weight iron and the oxygen paradox in isolated rat hearts. Voogd, A., Sluiter, W., van Eijk, H.G., Koster, J.F. J. Clin. Invest. (1992) [Pubmed]
  3. Hypothesis: is lung disease after silicate inhalation caused by oxidant generation? Ghio, A.J., Kennedy, T.P., Schapira, R.M., Crumbliss, A.L., Hoidal, J.R. Lancet (1990) [Pubmed]
  4. Three chemically distinct types of oxidants formed by iron-mediated Fenton reactions in the presence of DNA. Luo, Y., Han, Z., Chin, S.M., Linn, S. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  5. Renoprotective properties of angiotensin receptor blockers beyond blood pressure lowering. Izuhara, Y., Nangaku, M., Inagi, R., Tominaga, N., Aizawa, T., Kurokawa, K., van Ypersele de Strihou, C., Miyata, T. J. Am. Soc. Nephrol. (2005) [Pubmed]
  6. Free radical damage, iron, and Alzheimer's disease. Smith, M.A., Perry, G. J. Neurol. Sci. (1995) [Pubmed]
  7. Comparison of fenton and photo-fenton processes for livestock wastewater treatment. Park, J.H., Cho, I.H., Chang, S.W. Journal of environmental science and health. Part. B, Pesticides, food contaminants, and agricultural wastes. (2006) [Pubmed]
  8. Prooxidant states and tumor promotion. Cerutti, P.A. Science (1985) [Pubmed]
  9. Asbestos inhalation induces reactive nitrogen species and nitrotyrosine formation in the lungs and pleura of the rat. Tanaka, S., Choe, N., Hemenway, D.R., Zhu, S., Matalon, S., Kagan, E. J. Clin. Invest. (1998) [Pubmed]
  10. Rapid responses to oxidative stress mediated by iron regulatory protein. Pantopoulos, K., Hentze, M.W. EMBO J. (1995) [Pubmed]
  11. A Fenton reaction at the endoplasmic reticulum is involved in the redox control of hypoxia-inducible gene expression. Liu, Q., Berchner-Pfannschmidt, U., Möller, U., Brecht, M., Wotzlaw, C., Acker, H., Jungermann, K., Kietzmann, T. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  12. Prevention of postischemic cardiac injury by the orally active iron chelator 1,2-dimethyl-3-hydroxy-4-pyridone (L1) and the antioxidant (+)-cyanidanol-3. van der Kraaij, A.M., van Eijk, H.G., Koster, J.F. Circulation (1989) [Pubmed]
  13. High incidence of allelic loss on chromosome 5 and inactivation of p15INK4B and p16INK4A tumor suppressor genes in oxystress-induced renal cell carcinoma of rats. Tanaka, T., Iwasa, Y., Kondo, S., Hiai, H., Toyokuni, S. Oncogene (1999) [Pubmed]
  14. Increased production of urea hydrogen peroxide from Maillard reaction and a UHP-Fenton pathway related to glycoxidation damage in chronic renal failure. Moh, A., Sakata, N., Takebayashi, S., Tateishi, K., Nagai, R., Horiuchi, S., Chihara, J. J. Am. Soc. Nephrol. (2004) [Pubmed]
  15. Kinetics of paraquat and copper reactions with nitroxides: the effects of nitroxides on the aerobic and anoxic toxicity of paraquat. Goldstein, S., Samuni, A., Aronovitch, Y., Godinger, D., Russo, A., Mitchell, J.B. Chem. Res. Toxicol. (2002) [Pubmed]
  16. Killing of Bacillus subtilis spores by a modified Fenton reagent containing CuCl2 and ascorbic acid. Shapiro, M.P., Setlow, B., Setlow, P. Appl. Environ. Microbiol. (2004) [Pubmed]
  17. Molecular cloning and nucleotide sequence of cDNA for rat ornithine carbamoyltransferase precursor. Takiguchi, M., Miura, S., Mori, M., Tatibana, M., Nagata, S., Kaziro, Y. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  18. Monocyte expression of the human prointerleukin 1 beta gene (IL1B) is dependent on promoter sequences which bind the hematopoietic transcription factor Spi-1/PU.1. Kominato, Y., Galson, D., Waterman, W.R., Webb, A.C., Auron, P.E. Mol. Cell. Biol. (1995) [Pubmed]
  19. Copper-dependent formation of miscoding etheno-DNA adducts in the liver of Long Evans cinnamon (LEC) rats developing hereditary hepatitis and hepatocellular carcinoma. Nair, J., Sone, H., Nagao, M., Barbin, A., Bartsch, H. Cancer Res. (1996) [Pubmed]
  20. Hydroxyl radical formation by sickle erythrocyte membranes: role of pathologic iron deposits and cytoplasmic reducing agents. Repka, T., Hebbel, R.P. Blood (1991) [Pubmed]
  21. Hypothermia injury/cold-induced apoptosis--evidence of an increase in chelatable iron causing oxidative injury in spite of low O2-/H2O2 formation. Rauen, U., Petrat, F., Li, T., De Groot, H. FASEB J. (2000) [Pubmed]
  22. Protection by desferrioxamine and other hydroxamic acids against tetrachlorohydroquinone-induced cyto- and genotoxicity in human fibroblasts. Witte, I., Zhu, B.Z., Lueken, A., Magnani, D., Stossberg, H., Chevion, M. Free Radic. Biol. Med. (2000) [Pubmed]
  23. Oxidative mechanisms in the toxicity of metal ions. Stohs, S.J., Bagchi, D. Free Radic. Biol. Med. (1995) [Pubmed]
  24. Iron accumulation in Alzheimer disease is a source of redox-generated free radicals. Smith, M.A., Harris, P.L., Sayre, L.M., Perry, G. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  25. Micromolar intracellular hydrogen peroxide disrupts metabolism by damaging iron-sulfur enzymes. Jang, S., Imlay, J.A. J. Biol. Chem. (2007) [Pubmed]
  26. Iron-catalyzed hydroxyl radical formation. Stringent requirement for free iron coordination site. Graf, E., Mahoney, J.R., Bryant, R.G., Eaton, J.W. J. Biol. Chem. (1984) [Pubmed]
  27. Changes in the viscosity of hyaluronic acid after exposure to a myeloperoxidase-derived oxidant. Baker, M.S., Green, S.P., Lowther, D.A. Arthritis Rheum. (1989) [Pubmed]
  28. Scatchard analysis of methane sulfinic acid production from dimethyl sulfoxide: a method to quantify hydroxyl radical formation in physiologic systems. Babbs, C.F., Griffin, D.W. Free Radic. Biol. Med. (1989) [Pubmed]
  29. Growth inhibitory factor prevents neurite extension and the death of cortical neurons caused by high oxygen exposure through hydroxyl radical scavenging. Uchida, Y., Gomi, F., Masumizu, T., Miura, Y. J. Biol. Chem. (2002) [Pubmed]
  30. Mammalian 5-formyluracil-DNA glycosylase. 2. Role of SMUG1 uracil-DNA glycosylase in repair of 5-formyluracil and other oxidized and deaminated base lesions. Masaoka, A., Matsubara, M., Hasegawa, R., Tanaka, T., Kurisu, S., Terato, H., Ohyama, Y., Karino, N., Matsuda, A., Ide, H. Biochemistry (2003) [Pubmed]
  31. Heat shock-induced attenuation of hydroxyl radical generation and mitochondrial aconitase activity in cardiac H9c2 cells. Ilangovan, G., Venkatakrishnan, C.D., Bratasz, A., Osinbowale, S., Cardounel, A.J., Zweier, J.L., Kuppusamy, P. Am. J. Physiol., Cell Physiol. (2006) [Pubmed]
  32. Cellular prion protein regulates intracellular hydrogen peroxide level and prevents copper-induced apoptosis. Nishimura, T., Sakudo, A., Nakamura, I., Lee, D.C., Taniuchi, Y., Saeki, K., Matsumoto, Y., Ogawa, M., Sakaguchi, S., Itohara, S., Onodera, T. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  33. Mechanisms of Saccharomyces cerevisiae PMA1 H+-ATPase inactivation by Fe2+, H2O2 and Fenton reagents. Stadler, N., Höfer, M., Sigler, K. Free Radic. Res. (2001) [Pubmed]
  34. Involvement of a local fenton reaction in the reciprocal modulation by O2 of the glucagon-dependent activation of the phosphoenolpyruvate carboxykinase gene and the insulin-dependent activation of the glucokinase gene in rat hepatocytes. Kietzmann, T., Porwol, T., Zierold, K., Jungermann, K., Acker, H. Biochem. J. (1998) [Pubmed]
  35. Use of free radical chemistry in an immunometric assay for 17 beta-estradiol. Buscarlet, L., Volland, H., Dupret-Carruel, J., Jolivet, M., Grassi, J., Créminon, C., Taran, F., Pradelles, P. Clin. Chem. (2001) [Pubmed]
  36. Excimer laser-induced hydroxyl radical formation and keratocyte death in vitro. Shimmura, S., Masumizu, T., Nakai, Y., Urayama, K., Shimazaki, J., Bissen-Miyajima, H., Kohno, M., Tsubota, K. Invest. Ophthalmol. Vis. Sci. (1999) [Pubmed]
  37. Generation of putative intrastrand cross-links and strand breaks in DNA by transition metal ion-mediated oxygen radical attack. Lloyd, D.R., Phillips, D.H., Carmichael, P.L. Chem. Res. Toxicol. (1997) [Pubmed]
  38. Comparison of the formation of 8-hydroxy-2'-deoxyguanosine and single- and double-strand breaks in DNA mediated by fenton reactions. Lloyd, D.R., Carmichael, P.L., Phillips, D.H. Chem. Res. Toxicol. (1998) [Pubmed]
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