Production and reactions
In the finishing of steel prior to plating or coating, the steel sheet or rod is passed through pickling baths of sulfuric acid. This treatment produces large quantities of iron(II) sulfate as a by-product. Fe + H2SO4 → FeSO4 + H2Another source of large amounts results from the production of titanium dioxide from ilmenite via the sulfate process. Ferrous sulfate is also prepared commercially by oxidation of pyrite:
2 FeS2 + 7 O2 + 2 H2O → 2 FeSO4 + 2 H2SO4It can be produced by displacement of metals less reactive than Iron from solutions of their sulfate:

CuSO4 + Fe → FeSO4 + Cu

Reactions
Upon dissolving in water, ferrous sulfates form the metal aquo complex [Fe(H2O)6]2+, which is an almost colorless, paramagnetic ion. On heating, iron(II) sulfate first loses its water of crystallization and the original green crystals are converted into a white anhydrous solid. When further heated, the anhydrous material decomposes into sulfur dioxide and sulfur trioxide, leaving a reddish-brown iron(III) oxide. Thermolysis of iron(II) sulfate begins at about 680 °C (1,256 °F).
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase. It was first formally characterized in 1954. Presentation
Sufferers have unusually high concentrations of xanthine in their blood and urine, which can lead to health problems such as renal failure and xanthine kidney stones, one of the rarest types of kidney stones. Causes
Type I xanthinuria can be caused by a deficiency of xanthine oxidase, which is an enzyme necessary for converting xanthine to uric acid. Type II xanthinuria and molybdenum cofactor deficiency lack one or two other enzyme activities in addition to xanthine oxidase. Treatment
There is no specific treatment beyond maintaining a high fluid intake and avoiding foods that are high in purine. References
External links

Xanthinuria at NIHs Office of Rare Diseases