Mossbauer spectroscopy and ELISA studies reveal differences between. Parkinson's disease and control substantia nigra

被引:41
作者
Galazka-Friedman, J
Bauminger, ER
Koziorowski, D
Friedman, A
机构
[1] Warsaw Univ Technol, Fac Phys, PL-00662 Warsaw, Poland
[2] Hebrew Univ Jerusalem, Racah Inst Phys, IL-91904 Jerusalem, Israel
[3] Med Univ Warsaw, Dept Neurol, IL-02097 Warsaw, Poland
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2004年 / 1688卷 / 02期
关键词
Parkinson's disease; nigral iron; Mossbauer spectroscopy; ELISA; ferritin; oxidative stress;
D O I
10.1016/j.bbadis.2003.11.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The possible role of iron in the degeneration of nervous cells in Parkinson's disease (PD) was studied with the use of Mossbauer spectroscopy (MS) and enzyme-linked immunoabsorbent assay (ELISA). Mossbauer data were obtained at 90 and 4.1 K from 21 samples of control and 9 samples of parkinsonian substantia nigra (SN). Mossbauer spectra were very similar to those observed in ferritin. Small differences were detected between the spectra obtained from PD and from control SN, and could be due to a slight difference in the composition of the ferritin-like iron cores or due to the presence of about 8% of non-ferritin-like iron in parkinsonian SN. ELISA studies from 11 controls and 6 parkinsonian SN showed a decrease in the concentration of L-chains in wet tissues of PD-SN compared to control SN. The decrease in the amount of L subunits may correspond to a decreased ability of this ferritin to keep iron in a safe form. Iron released from ferritin or neuromelanin (NM) may be the source of such iron, which may cause the difference in the Mossbauer spectra and may trigger oxidative stress leading to cell death. (C) 2003 Elsevier B.V. All rights reserved.
引用
收藏
页码:130 / 136
页数:7
相关论文
共 38 条
[1]   EPR investigations of the iron domain in neuromelanin [J].
Aime, S ;
Bergamasco, B ;
Biglino, D ;
Digilio, G ;
Fasano, M ;
Giamello, E ;
Lopiano, L .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1997, 1361 (01) :49-58
[2]   A MUTATIONAL ANALYSIS OF THE EPITOPES OF RECOMBINANT HUMAN H-FERRITIN [J].
AROSIO, P ;
COZZI, A ;
INGRASSIA, R ;
LEVI, S ;
LUZZAGO, A ;
RUGGERI, G ;
IACOBELLO, C ;
SANTAMBROGIO, P ;
ALBERTINI, A .
BIOCHIMICA ET BIOPHYSICA ACTA, 1990, 1039 (02) :197-203
[3]   MOSSBAUER SPECTROSCOPIC STUDIES OF HUMAN HEMOSIDERIN AND FERRITIN [J].
BELL, SH ;
WEIR, MP ;
DICKSON, DPE ;
GIBSON, JF ;
SHARP, GA ;
PETERS, TJ .
BIOCHIMICA ET BIOPHYSICA ACTA, 1984, 787 (03) :227-236
[4]   Magnetic investigations of human mesencephalic neuromelanin [J].
Bolzoni, F ;
Giraudo, S ;
Lopiano, L ;
Bergamasco, B ;
Fasano, M ;
Crippa, PR .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2002, 1586 (02) :210-218
[5]   Mineralization in ferritin: An efficient means of iron storage [J].
Chasteen, ND ;
Harrison, PM .
JOURNAL OF STRUCTURAL BIOLOGY, 1999, 126 (03) :182-194
[6]   The effect of histological processing on the form of iron in iron-loaded human tissues [J].
Chuaanusorn, W ;
Webb, J ;
Macey, DJ ;
Pootrakul, P ;
StPierre, TG .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1997, 1360 (03) :255-261
[7]   Neuropathological examination suggests impaired brain iron acquisition in restless legs syndrome [J].
Connor, JR ;
Boyer, PJ ;
Menzies, SL ;
Dellinger, B ;
Allen, RP ;
Ondo, WG ;
Earley, CJ .
NEUROLOGY, 2003, 61 (03) :304-309
[8]  
CONNOR JR, 1995, J NEUROCHEM, V65, P717
[9]   DECREASED FERRITIN LEVELS IN BRAIN IN PARKINSONS-DISEASE [J].
DEXTER, DT ;
CARAYON, A ;
VIDAILHET, M ;
RUBERG, M ;
AGID, F ;
AGID, Y ;
LEES, AJ ;
WELLS, FR ;
JENNER, P ;
MARSDEN, CD .
JOURNAL OF NEUROCHEMISTRY, 1990, 55 (01) :16-20
[10]   NEW DATA AND A REVISED STRUCTURAL MODEL FOR FERRIHYDRITE [J].
EGGLETON, RA ;
FITZPATRICK, RW .
CLAYS AND CLAY MINERALS, 1988, 36 (02) :111-124