The effects of two physiological low molecular weight iron complexes,
ferric lactate and ferric adenosine triphosphate (ATP) on brain Ca2+ h
omeostasis modification, have been studied in vitro and in vivo. In vi
tro ferric ATP complex shows a higher efficiency as modifier of Ca2+ h
omeostasis. This higher reactivity and the in vivo observed effect of
increased brain uptake of iron from ferric lactate provoked by the pre
sence of ATP, corroborate in vitro results showing an iron transfer fr
om ferric lactate to ATP, as well as the mediator role of ATP in the i
ron-induced cellular Ca2+ homeostasis modification process. The possib
le role of this process in Parkinson's disease is discussed.