Magnesium, Ceruloplasmin & Iron Management

There are 3,571 proteins that Require Magnesium to do their job and key to an optimal Iron management is a sufficient amount of a (magnesium dependent) protein called Ceruloplasmin.

That's how the human body works. Enzymes/proteins ARE RULED by minerals and hormones are ruled by enzymes/proteins, NOT the other way around!
Every bio-chemical process in our body needs a signal to get started and such signals come from minerals like Magnesium, which is the Master Mineral.

Without Magnesium there would be NO life on earth.

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Major targets of iron-induced protein oxidative damage in frataxin-deficient yeasts are magnesium-binding proteins.
Irazusta V, et al. Free Radic Biol Med. 2008.

Abstract
Iron accumulation has been associated with several pathological conditions such as Friedreich ataxia. This human disorder is caused by decreased expression of frataxin. Iron-overload triggers oxidative stress, but the main targets of such stress are not known. In yeast cells lacking the frataxin ortholog YFH1, we have identified a set of 14 carbonylated proteins, which include mitochondrial ATP synthase, phosphoglycerate kinase, pyruvate kinase, and molecular chaperones. Interestingly, most of the target proteins are magnesium- and/or nucleotide-binding proteins. This key feature leads us to postulate that when iron accumulates, chelatable iron replaces magnesium at the corresponding metal-binding site, promoting selective damage to these proteins. Consistent with this hypothesis, in vitro experiments performed with pure pyruvate kinase and phosphoglycerate kinase showed that oxidation of these proteins can be prevented by magnesium and increased by the presence of ATP. Also, chelatable iron, which forms complexes with nucleotides, showed a sevenfold increase in Deltayfh1 cells. Moreover, lowering chelatable iron in Deltayfh1 cells by desferrioxamine prevented enzyme inactivation. As a general conclusion, we propose that magnesium bound to proteins is replaced by chelatable iron when this metal accumulates. This mechanism explains selective protein oxidation and provides clues for better understanding of iron-overloading pathologies.
http://www.sciencedirect.com/science/article/pii/S0891584908000294?via%3Dihub