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Chemical Compound Review

Molysite     trichloroiron

Synonyms: FeCl3, TDA REAGENT, HSDB 449, CCRIS 2299, Flores martis, ...
 
 
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Disease relevance of trichloroiron

 

High impact information on trichloroiron

  • Neither FeCl3 in combinations with H2O2, nor Fe3+ or Fe2+ chelated with EDTA, nor Zn2+-protoporphyrin IX, nor protoporphyrin IX caused significant inactivation of FRP [6].
  • Thus, iron bound to lactoferrin was approximately 5,000 times more effective in producing an enhancement in ethylene generation than iron derived from FeCl3 or ferric EDTA [7].
  • Whole-blood clotting times and FeCl3 carotid artery injury correction demonstrated that platelet FVIII demonstrably improved the bleeding diathesis in FVIIInull mice independent of the platelets' VWF status [8].
  • In a cuticular bleeding time study, these animals also had only a partial correction, but in an FeCl3 carotid artery, thrombosis assay correction was equivalent to a 50% to 100% level [9].
  • We used the whole-cell variant of the patch-clamp technique to study sustained depolarization in guinea pig ventricular myocytes during the extracellular application of O-Rs (generating system: dihydroxyfumaric acid, 3 to 6 mmol/L; FeCl3/ADP, 0.05:0.5 mmol/L) [10].
 

Chemical compound and disease context of trichloroiron

  • Heparin (1000 U), when given i.v. after FeCl3, did not affect the thrombus size per se, but caused a reduction in the interindividual variation of the size of the thrombus (p < 0.05) [11].
  • Tranexamic acid (50 mg/kg), an inhibitor of fibrinolysis, increased thrombus size (p = 0.014) when given intravenously (i.v.) prior to the FeCl3-exposure [11].
  • Subtoxic FeCl3 (500 mg/dl) was concurrently added to identical cultures to determine if deferoxamine potentiated iron toxicity [12].
  • Each sample, original or coated by TETA, was exposed to oxygen, 1 x 10(-3) M FeCl3, and Acidithiobacillus ferrooxidans, respectively, for specific oxidation periods [13].
  • Inactivation of Klebsiella pneumoniae cultures by chlorine and chloramine was evaluated under different growth conditions by varying nutrient media dilution, concentrations of essential inorganic nutrients (FeCl3, MgSO4, phosphate, and ammonium salts), and temperature [14].
 

Biological context of trichloroiron

  • DNA damage after the addition of electron donors alone or with FeCl3 or DFO-Fe3+ was not visualized [15].
  • In normal Purkinje fibres, FeCl3/ADP (0.1/1.0 microM) induced a decrease in action potential duration without any pronounced effect on Vmax, diastolic potential, and activation potential [16].
  • Chemical hypoxia-evoked cell death and LDH release were counteracted by the ferricyanide moiety of the SNP molecule, K3Fe(CN)6, and by ferric chloride (FeCl3), and this effect was counteracted by CB-DMB [17].
  • A number of the compounds exhibited good oral bioavailability in rats and dogs, and numerous compounds were efficacious in a rat FeCl3-induced model of arterial thrombosis [18].
  • Selective oxidative cyclization by FeCl3 in the construction of 10H-indeno[1,2-b]triphenylene skeletons in polycyclic aromatic hydrocarbons [19].
 

Anatomical context of trichloroiron

  • Highly purified sarcolemmal membranes, isolated from canine ventricular myocytes, were peroxidized by a superoxide anion-producing and iron-catalyzed free radical-generating system (dihydroxy-fumarate plus FeCl3 and ADP) [20].
  • Inhibition of mineralization of glutaraldehyde-pretreated bovine pericardium by AlCl3. Mechanisms and comparisons with FeCl3, LaCl3, and Ga(NO3)3 in rat subdermal model studies [21].
  • A filter soaked in 29% FeCl3 was applied around the abdominal aorta to study the patterns of arterial thrombosis [22].
  • Human monocyte-derived macrophages (HMDMs) were isolated and cultured for 7 days and then exposed to FeCl3, Fe-ADP, or Fe-EDTA (100 mumol/L) or hemoglobin (25 or 50 micrograms/mL) for 24 hours [23].
  • Thus the results indicated that: (1) certain porphyrogenic agents increased ALA synthase mass and RNA in chick-embryo intestine and kidney, in addition to liver; (2) ALA and FeCl3 inhibited the elevations; and (3) the sizes of ALA synthase's subunit as well as the enzyme's mRNA appeared identical, in each case, in all tissues examined [24].
 

Associations of trichloroiron with other chemical compounds

 

Gene context of trichloroiron

  • FXI is essential for thrombus formation following FeCl3-induced injury of the carotid artery in the mouse [29].
  • In contrast, these data show that tonB transcription is repressed threefold by growth in the presence of FeCl3 compared with growth in the presence of the iron chelator dipyridyl and that this repression requires the fur locus [30].
  • In order to inhibit the binding of 67Ga to transferrin in the blood, FeCl3 was administered 5 min before the injection of 67Ga [31].
  • BLM, FeCl3, cytochrome b5 and NADH were absolutely necessary to provide these effects [32].
  • Exogenous iron concentration in culture was manipulated by supplementing the medium with sera having different iron concentrations over the range 0.6 to 5.4 micrograms/ml, by the addition of iron in the form of FeCl3, iron-saturated serum, or diferric transferrin, and by the addition of the iron chelator Desferal (desferrioxamine) [33].
 

Analytical, diagnostic and therapeutic context of trichloroiron

  • The polymers induced by FeCl3 did not enter the spacer gel, and those induced by CuSO4 migrated to the top of the running gel, indicating that the former polymers were larger than the latter, which in gel filtration experiments appeared to be larger than Mr 670,000 [26].
  • Effects of the free radical generating system FeCl3/ADP on reperfusion arrhythmias of rat hearts and electrical activity of canine Purkinje fibres [16].
  • Perfusion of 800 fmol FeCl3/15 min along with 40 nmol MPP+ and 400 fmol DES on day 1 completely abolished on day 2 the neuroprotective effect found with 40 nmol MPP+ and 400 fmol DES; 800 fmol FeCl3 did not increase the neurotoxic effect of 40 nmol MPP+ perfusion [34].
  • In the second part of this study the electrophysiological effects of FeCl3/ADP (0.1/1.0 microM) were investigated in normal Purkinje fibres and in Purkinje fibres from dog surviving infarction, by using conventional microelectrode method [16].
  • We also examined the effect of melatonin on the appearance of epileptic discharges in the EEG following injection of FeCl3 into the sensorimotor cortex in anesthetized rats, and by measuring the concentration of TBARS in the brain tissue [35].

References

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  3. Free radical scavenging action of Bio-catalyzer alpha.rho No.11 (Bio-normalyzer) and its by-product. Santiago, L.A., Osato, J.A., Hiramatsu, M., Edamatsu, R., Mori, A. Free Radic. Biol. Med. (1991) [Pubmed]
  4. Bactericidal activity of M14659 enhanced in low-iron environments. Mochizuki, H., Yamada, H., Oikawa, Y., Murakami, K., Ishiguro, J., Kosuzume, H., Aizawa, N., Mochida, E. Antimicrob. Agents Chemother. (1988) [Pubmed]
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  10. Oxygen-derived free radical stress activates nonselective cation current in guinea pig ventricular myocytes. Role of sulfhydryl groups. Jabr, R.I., Cole, W.C. Circ. Res. (1995) [Pubmed]
  11. The Fab-fragment of a PAI-1 inhibiting antibody reduces thrombus size and restores blood flow in a rat model of arterial thrombosis. van Giezen, J.J., Wahlund, G., Nerme, n.u.l.l., Abrahamsson, T. Thromb. Haemost. (1997) [Pubmed]
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  13. The passivation of pyrrhotite by surface coating. Cai, M.F., Dang, Z., Chen, Y.W., Belzile, N. Chemosphere (2005) [Pubmed]
  14. Factors influencing inactivation of Klebsiella pneumoniae by chlorine and chloramine. Goel, S., Bouwer, E.J. Water Res. (2004) [Pubmed]
  15. Nuclear DNA damage during NAD(P)H oxidation by membrane redox chains. Peskin, A.V. Free Radic. Biol. Med. (1996) [Pubmed]
  16. Effects of the free radical generating system FeCl3/ADP on reperfusion arrhythmias of rat hearts and electrical activity of canine Purkinje fibres. Bril, A., Rochette, L., Verry, A., Maupoil, V., Man, R.Y., Opie, L.H. Cardiovasc. Res. (1990) [Pubmed]
  17. Sodium nitroprusside prevents chemical hypoxia-induced cell death through iron ions stimulating the activity of the Na+-Ca2+ exchanger in C6 glioma cells. Amoroso, S., Tortiglione, A., Secondo, A., Catalano, A., Montagnani, S., Di Renzo, G., Annunziato, L. J. Neurochem. (2000) [Pubmed]
  18. Synthesis of a series of potent and orally bioavailable thrombin inhibitors that utilize 3,3-disubstituted propionic acid derivatives in the P3 position. Tucker, T.J., Lumma, W.C., Lewis, S.D., Gardell, S.J., Lucas, B.J., Sisko, J.T., Lynch, J.J., Lyle, E.A., Baskin, E.P., Woltmann, R.F., Appleby, S.D., Chen, I.W., Dancheck, K.B., Naylor-Olsen, A.M., Krueger, J.A., Cooper, C.M., Vacca, J.P. J. Med. Chem. (1997) [Pubmed]
  19. Selective oxidative cyclization by FeCl3 in the construction of 10H-indeno[1,2-b]triphenylene skeletons in polycyclic aromatic hydrocarbons. Zhou, Y., Liu, W.J., Zhang, W., Cao, X.Y., Zhou, Q.F., Ma, Y., Pei, J. J. Org. Chem. (2006) [Pubmed]
  20. Comparative antioxidant activities of propranolol, nifedipine, verapamil, and diltiazem against sarcolemmal membrane lipid peroxidation. Mak, I.T., Weglicki, W.B. Circ. Res. (1990) [Pubmed]
  21. Inhibition of mineralization of glutaraldehyde-pretreated bovine pericardium by AlCl3. Mechanisms and comparisons with FeCl3, LaCl3, and Ga(NO3)3 in rat subdermal model studies. Webb, C.L., Schoen, F.J., Flowers, W.E., Alfrey, A.C., Horton, C., Levy, R.J. Am. J. Pathol. (1991) [Pubmed]
  22. Differential effects of alpha- and gamma-tocopherol on low-density lipoprotein oxidation, superoxide activity, platelet aggregation and arterial thrombogenesis. Saldeen, T., Li, D., Mehta, J.L. J. Am. Coll. Cardiol. (1999) [Pubmed]
  23. Effects of iron- and hemoglobin-loaded human monocyte-derived macrophages on oxidation and uptake of LDL. Yuan, X.M., Brunk, U.T., Olsson, A.G. Arterioscler. Thromb. Vasc. Biol. (1995) [Pubmed]
  24. Regulation of production of delta-aminolaevulinate synthase in tissues of chick embryos. Effects of porphyrogenic agents and of haem precursors. Drew, P.D., Ades, I.Z. Biochem. J. (1989) [Pubmed]
  25. Non-transferrin-bound iron in plasma or serum from patients with idiopathic hemochromatosis. Characterization by high performance liquid chromatography and nuclear magnetic resonance spectroscopy. Grootveld, M., Bell, J.D., Halliwell, B., Aruoma, O.I., Bomford, A., Sadler, P.J. J. Biol. Chem. (1989) [Pubmed]
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  27. NADH- and NADPH-dependent lipid peroxidation in bovine heart submitochondrial particles. Dependence on the rate of electron flow in the respiratory chain and an antioxidant role of ubiquinol. Takayanagi, R., Takeshige, K., Minakami, S. Biochem. J. (1980) [Pubmed]
  28. Iron-induced DNA damage and synthesis in isolated rat liver nuclei. Shires, T.K. Biochem. J. (1982) [Pubmed]
  29. FXI is essential for thrombus formation following FeCl3-induced injury of the carotid artery in the mouse. Rosen, E.D., Gailani, D., Castellino, F.J. Thromb. Haemost. (2002) [Pubmed]
  30. Aerobic regulation of the Escherichia coli tonB gene by changes in iron availability and the fur locus. Postle, K. J. Bacteriol. (1990) [Pubmed]
  31. Transferrin is not involved in the entry of 67Ga into hepatocytes from regenerating liver of partially hepatectomized rats. Abe, S., Hasegawa, S., Nirasawa, M., Sasaki, M., Ohkubo, Y. Biol. Pharm. Bull. (2001) [Pubmed]
  32. Redox cycling of bleomycin-Fe(III) and DNA degradation by isolated NADH-cytochrome b5 reductase: involvement of cytochrome b5. Mahmutoglu, I., Kappus, H. Mol. Pharmacol. (1988) [Pubmed]
  33. Regulation of K562 cell transferrin receptors by exogenous iron. Rudolph, N.S., Ohlsson-Wilhelm, B.M., Leary, J.F., Rowley, P.T. J. Cell. Physiol. (1985) [Pubmed]
  34. Neuroprotective effect of the iron chelator desferrioxamine against MPP+ toxicity on striatal dopaminergic terminals. Santiago, M., Matarredona, E.R., Granero, L., Cano, J., Machado, A. J. Neurochem. (1997) [Pubmed]
  35. Melatonin inhibits iron-induced epileptic discharges in rats by suppressing peroxidation. Kabuto, H., Yokoi, I., Ogawa, N. Epilepsia (1998) [Pubmed]
 
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