Involvement of iron ions in 6-hydroxydopamine-induced disruption of intracellular copper metabolism.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. Recently, disorders in metabolism of metals, including copper (Cu) and iron (Fe), have been reported to be linked to the pathogenesis of PD. We previously demonstrated that 6-hydoroxydopamine (6-OHDA), a neurotoxin used for the production of PD model animals, decreases Atox1, a Cu chaperone, and ATP7A, a Cu transporter, and disrupts intracellular Cu metabolism in human neuroblastoma SH-SY5Y cells.

6-Hydroxydopamine disrupts cellular copper homeostasis in human neuroblastoma SH-SY5Y cells.

Copper (Cu) is an essential trace element that plays an important role in maintaining neuronal functions such as the biosynthesis of neurotransmitters. In contrast, exposure to excess Cu results in cell injury. Therefore, intracellular Cu levels are strictly regulated by proteins related to Cu-trafficking, including ATP7A.