Parkinson's disease is one of the most frequent human neurodegenerations. Motor symptoms of Parkinson's disease are the consequence of the destruction of nervous cells in the substantia nigra (SN), a small (about 500 mg) structure located deep in human brain. The concentration of iron in SN is comparable to that in liver and is equal to about 180 ? 60 ng/mg of wet tissue and the iron in SN is mostly bound to ferritin. For many years it has been believed that the degeneration of nervous cells in SN in Parkinson's disease is related to an important increase in the concentration of iron. Our own studies based on M?ssbauer spectroscopy and other studies conducted with the use of various techniques have not confirmed this finding. The ratio of the concentration of iron in PD vs. control SN evaluated by Mossbauer spectroscopy was found to be equal 1.00?0.13. We also confirmed that most of iron in SN is located within ferritin. ELISA studies demonstrated a significant decrease in L ferritin in parkinsonian SN compared to the control group. As L-ferritin is related to safe keeping of iron within the ferritin shell, its decrease may lead to an efflux of iron and increase in the concentration of labile iron. Indeed our studies did show a difference in the concentration of labile iron between PD and control SN (135 +- 10 ng/g vs. 76 +- 5 ng/g). This labile iron, which may initiate Fenton reaction, may be the cause of the oxidative stress leading to the death of nervous cells in PD.
According to the oxidative stress theory iron may play an important role in the pathogenesis of neurodegenerative diseases, as e.g. Parkinson's disease (PD). This review presents the results of studies, obtained by various methods, of iron in substantia nigra (SN) - a cerebral structure which degenerates in PD - and shows controversies concerning the amount of iron, its redox state, and the iron binding compounds. Taking into account all published experimental results, the increase in the concentration of iron in parkinsonian SN vs. control may be estimated as (3 + - 5)%. The presence of large amounts of divalent iron in post mortem SN can be unequivocally negated. It is, however, still possible that iron is involved in the pathogenesis of PD, as even minor changes in the amount and form of iron may initiate processes leading to cells death.
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