Iron metabolism and Parkinson's disease.
There are at least three major reasons for thinking that iron participates in the mechanism of nerve cell death in Parkinson's disease (PD): (1) Iron catalyzes the formation of highly toxic hydroxyl radicals through the Fenton reaction. (2) Evidence suggests that oxidative stress participates in the mechanism of nerve cell death in PD. (3) Increased iron concentrations have been observed in the substantia nigra of patients with PD. In this review, we report data suggesting that the vulnerable neurons in PD are particularly sensitive to oxidative stress that may be induced by iron and then discuss the mechanisms by which iron levels may be increased in dopaminergic neurons in PD.
Hirsch
E C
EC
INSERM U289, Hôpital de la Salpêtrière, Paris, France.
Faucheux
B A
BA
D016923:Cell Death / Q000502:physiology*; D004298:Dopamine / Q000502:physiology; D005609:Free Radicals; D006801:Humans; D017665:Hydroxyl Radical / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D007781:Lactoferrin / Q000378:metabolism; D009474:Neurons / Q000473:pathology; D010300:Parkinson Disease / Q000473:pathology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013378:Substantia Nigra / Q000473:pathology; D014168:Transferrin / Q000378:metabolism
D005609:Free Radicals; D017382:Reactive Oxygen Species; D014168:Transferrin; D017665:Hydroxyl Radical; D007501:Iron; D007781:Lactoferrin; D004298:Dopamine