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Iron fluoride can refer to
Iron(II) fluoride (ferrous fluoride, FeF2), a white solid
Iron(III) fluoride (ferric fluoride, FeF3), a pale green solid
Iron(II) fluoride (also ferrous fluoride) is a chemical compound with formula FeF2. It is a green crystalline solid that melts at about 1000°C. It is used in ceramics and as a catalyst in some organic reactions.
The anhydrous salt can be prepared by reacting the elements. It has the TiO2 rutile structure where the iron atoms are octahedrally coordinated and the fluoride ions three coordinate.
Iron(III) fluoride, also known as ferric fluoride, is an inorganic compound. It exists in an anhydrous form (formula FeF3) as well as two hydrated forms (both formula FeF3·3H2O). It is produced commercially mostly for laboratory work and is not as useful as the related compound iron(III) chloride. Anhydrous iron(III) fluoride is white while the hydrated forms are light pink.
Preparation, occurrence, reactions
Anhydrous iron(III) fluoride is prepared by treating virtually any anhydrous iron compound with fluorine. More practically and like most metal fluorides, it is prepared by treating the corresponding chloride with hydrogen fluoride:
FeCl3 + 3 HF → FeF3 + 3 HCl
It also forms as a passivating film upon contact between iron (and steel) and hydrogen fluoride. The hydrates crystallize from aqueous hydrofluoric acid.
The material is a fluoride acceptor. With xenon hexafluoride it forms [FeF4]XeF5].
The A53T α-Synuclein Mutation Increases Iron-Dependent Aggregation and Toxicity
Natalie Ostrerova-Golts1, Leonard Petrucelli1, John Hardy3, John M. Lee1,2, Matthew Farer3, and Benjamin Wolozin1
+ Author Affiliations
1 Departments of Pharmacology and
2 Pathology, Loyola University Medical Center, Maywood, Illinois 60153, and
3 Department of Pharmacology, Mayo Clinic, Jacksonville, Florida 32224
Parkinson's disease (PD) is the most common motor disorder affecting the elderly. PD is characterized by the formation of Lewy bodies and death of dopaminergic neurons. The mechanisms underlying PD are unknown, but the discoveries that mutations in α-synuclein can cause familial PD and that α-synuclein accumulates in Lewy bodies suggest that α-synuclein participates in the pathophysiology of PD.
Using human BE-M17 neuroblastoma cells overexpressing wild-type, A53T, or A30P α-synuclein, we now show that iron and free radical generators, such as dopamine or hydrogen peroxide, stimulate the production of intracellular aggregates that contain α-synuclein and ubiquitin. The aggregates can be identified by immunocytochemistry, electron microscopy, or the histochemical stain thioflavine S. The amount of aggregation occurring in the cells is dependent on the amount of α-synuclein expressed and the type of α-synuclein expressed, with the amount of α-synuclein aggregation following a rank order of A53T > A30P > wild-type > untransfected.
In addition to stimulating aggregate formation, α-synuclein also appears to induce toxicity. BE-M17 neuroblastoma cells overexpressing α-synuclein show up to a fourfold increase in vulnerability to toxicity induced by iron. The vulnerability follows the same rank order as for aggregation. These data raise the possibility that α-synuclein acts in concert with iron and dopamine to induce formation of Lewy body pathology in PD and cell death in PD.
Astronauts In Space For More Than One Month 'Suffer Brain And Eye Damage'
Huffington Post UK Sara C Nelson
First Posted: 13/03/2012 12:35 Updated: 13/03/2012 12:35
Astronauts who have spent more than a month in space have shown evidence of damage to their eyeballs and brain tissue.
MRI scans on 27 Nasa astronauts revealed a pattern of deformities in their eyeballs, optic nerves and pituitary glands, it was revealed in the journal Radiology.
Seven of the astronauts had a flattening of one or both of the eyeballs, causing them to become long-sighted.