Revision as of 11:54, 3 October 2013

Iron coli project

Seminar on hemochromatosis the 18^th of September

On the 18^th of September, Evry iGEM team organized a seminar on hemochromatosis on iron related diseases. The aim of this seminar is to present the latest scientific advances on thoses diseases and futur treatments. We also take this opportunity to present synthetic biology and our project in iGEM competition to both scientists and patients.

Day's agenda

Start time	Speaker	Subject
10:00	Gabriel Guillocheau	Opening speech
10:15	PHD-DR Gaël Nicolas	Iron homeostasis in mammals and its deregulation
11:00	PU-PH Pierre Brissot	Hemochromatosis: its diagnostic and its treatment
11:45	Break
12:00	Docteur Marie-Paule Roth	Link between HFE, hepcidin and BMP6
12:45	Lunch
14:15	Result questionnaire with patients participation
15::00	Nicolas Pollet	Microbiom studies
15:45	Break
16:00	iGEM EVRY team	A bacterial treatment for hemochromatosis
16:45	Gabriel Guillocheau	Closing speech

Report of the day

Gaël Nicolas: "Iron homeostasis in mammals and its deregulation"

Summary

Iron is necessary to living beings but potentially toxic, that is why homeostasis is required. In a human body there are 4g to 5g of iron, that is about a rusted nail. Iron is present as Fe2+ and Fe3+; as Fe3+ it is insoluble and thus must be degraded in Fe2+, but as Fe2+ it becomes highly toxic because it is a strong oxidant. Much of iron is located in the red blood cells. This explains why we associate iron with oxygen transport, but many other reactions imply iron.
In the 1930's, an experiment showed that iron was not excreted by the body: iron remains stocked in the body. We absorb 1mg to 2mg of iron daily in order to compensate 1mg to 2 mg of iron lost daily through the death of cells. The production of red blood cells uses 20mg of iron daily, but these 20mg exclusively come from the recycling process of old red blood cells by macrophages.
Hepcidin is a hormone that makes the level of iron in the serum decrease. Hepcidin is thus to iron approximatively what insulin is to glucose. Its deficiency is implied in almost all the forms of hemochromatosis. This hormone has three sulphur bridges, that makes it very difficult to synthesise.

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