Who's to say high doses of anti-oxidants won't be preventing proper oxidation of ferrous in body thus resulting in improper heme production which causes you to have a decreased production of cytochrome P450s thus resulting in buildup of toxic substance in the body resulting in multi-system failure?
This is prolly not true, but doesn't mean something else like that can't be true
I currently work in the hematology and iron metabolism field (and I'm a huge nerd
), so just cannot help but interject here. (Don't worry, I still realize you were being mostly facietious, but hey, I get excited about my research!
)
Oxidation of newly exported ferrous iron (Fe2+) is handled almost exclusively by two specific ferroxidase proteins. The body specifically ensures this via protein oxidases because only ferric iron (Fe3+) can be efficiently bound to plasma transferrin (the major iron carrier), but in order to be transported to the plasma, iron must be in the Fe2+ form.
Iron (Fe2+) exported to the plasma originating from duodenal enterocytes is oxidized to Fe3+ by a membrane bound protein "Haphaestin". Haphaestin associates with ferroportin (the only known iron exporter) on the enterocyte surface and ensures that exported Fe2+ is almost immediately oxidized to Fe3+. In fact, without Haphaestin, ferroportin will not export iron at all.
In reticuloendothelial macrophages that recycle iron from senescent red blood cells, there is a ferroxidase called "Ceruloplasmin" that has the exact same job as Haphaestin in enterocytes. Ceruloplasmin is actually a plasma ferroxidase that associates with membrane ferroportin. So the net effect is the same. Fe2+ is almost immediately converted to Fe3+ and then bound to plasma transferrin.
/end dork rant.
