Disease relevance of trichloroiron

• FeCl3 was used to induce carotid artery thrombosis [1].
• Antioxidant action of guilingji in the brain of rats with FeCl3-induced epilepsy [2].
• Vivo tests showed that oral administration of 1-g/kg body weight of Bio-catalyzer significantly inhibited thiobarbituric acid reactive substances formation, which is an index of lipid peroxidation, in the FeCl3-induced epileptic focus of rats [3].
• The E. coli used in this study was confirmed to derepress iron transport systems in the presence of transferrin, lactoferrin, and alpha,alpha'-dipyridyl and in the iron-deficient Mueller-Hinton broth supplemented with FeCl3 at 0 to 1.0 microM [4].
• We investigated the if vivo effects of intravenous magnesium administration in a rat model of chemically induced (FeCl3) carotid thrombosis [5].

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

• HPLC analysis rigorously confirmed the presence of an iron-citrate complex in ultrafiltrates of plasma or serum studies with added FeCl3 or desferrioxamine supported this conclusion [25].
• When incubated in the presence of FeCl3, the Mr 30,000 NH2-terminal, Mr 40,000 gelatin-binding, and the Mr 120,000-140,000 COOH-terminal fragments of fibronectin formed disulfide-bonded polymers, whereas only the Mr 140,000 fragment was polymerized in the presence of CuSO4 [26].
• Disulfide-bonded polymers were also formed in the presence of FeCl3 but not CuSO4 when the free sulfhydryl groups of fibronectin were blocked by N-ethylmaleimide [26].
• Malondialdehyde formations by bovine heart submitochondrial particles supported by NADH or NADPH in the presence of ADP and FeCl3 was studied [27].
• Lipid peroxidation took place in nuclei incubated with FeCl2, but not with FeCl3 [28].

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