J. Lan et Dh. Jiang, EXCESSIVE IRON ACCUMULATION IN THE BRAIN - A POSSIBLE POTENTIAL RISK OF NEURODEGENERATION IN PARKINSONS-DISEASE, Journal of neural transmission, 104(6-7), 1997, pp. 649-660
In this study a chronic cerebral iron-loaded model was established by
feeding mice with high iron diet. Data indicated that brain iron conce
ntrations were significantly increased in iron-fed mice compared with
those of controls. A significant increase in oxidized glutathione (GSS
G), decrease in total glutathione (oxidized and reduced glutathione, G
SSG + GSH), and therefore increase in the GSSG/(GSSG + GSH) ratios wer
e observed in iron-loaded mice. Hydroxyl radical ((OH)-O-.) levels in
striatum and brainstem were also significantly increased. Excessive ir
on alone did not change either dopamine (DA) or lipid peroxidation (LP
O) concentrations in striatum. However, a single injection of 1-methyl
-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg, i.p.) into the i
ron-loaded mice caused a great enhancement in all these biochemical ab
normalities. These findings suggest that iron does induce oxidative st
ress, but not severely injury neurons per se. Excessive iron accumulat
ion in the brain, however, is a potential risk for neuronal damage, wh
ich may promote by triggering factor(s). This supports the hypothesis
that excessive cerebral iron may contribute to the aetiology of Parkin
son's disease (PD).