Elevated iron levels in the substantia nigra (SN) participate in neuronal death in Parkinson's disease (PD). While the mechanisms underlying the increased iron are still unknown, some iron transport proteins may be involved. The nigral iron accumulation could be a result of either increased import or decreased export. The mechanisms of iron import have received considerable attention, but little is known about iron export mechanisms. Ferroportin1 (FP1) and hephaestin (HP), two newly discovered iron export proteins, cooperate in the iron export in the gut. Here, we investigated their expression in the SN of rats lesioned by 6-hydroxydopamine (6-OHDA). Using immunofluorescence, we showed that FP1 and HP were both expressed on astrocytes, microglia, oligodendrocytes and neurons in the SN. By immunohistochemistry, we showed that 1 day after 6-OHDA lesion, the expression of the two proteins decreased compared with the control. When rats began showing rotation behaviour induced by apomorphine, usually 6 weeks after 6-OHDA lesion, they are considered PD models. In these PD models, a further decrease in the two proteins was observed. Reverse transcriptase-polymerase chain reaction showed that the mRNA levels of FP1 and HP decreased 1 day after 6-OHDA lesion compared with the control, and further decrease was also observed in the PD model rats. These results show for the first time that FP1 and HP co-localize in the rat brain, and suggest that decreased expression of these transporters in the SN can account for the increased iron levels.