The bloodstream form of Trypanosoma brucei acquires iron from transferrin by receptor-mediated endocytosis. However, it is unknown how procyclic forms that cannot bind transferrin acquire iron. Here, we show that the procyclic form of T. brucei efficiently takes up iron from ferric complexes via a reductive mechanism and that iron obtained using this mechanism is transported to, and used in, the mitochondria. The affinity of the transport system is comparable to that of Saccharomyces cerevisiae, with an apparent K_m of 0.85 μM.