Effect of aluminum on iron-induced lipid peroxidation and protein oxidative modification of mouse brain homogenate

被引:18
作者
Toda, S
Yase, Y
机构
[1] Kansai Coll Oriental Med, Dept Biochem, Osaka 59004, Japan
[2] Kansai Coll Oriental Med, Res Ctr Neurol Disorders, Osaka 59004, Japan
关键词
aluminum(III); brain homogenate; EDTA; iron(II); lipid peroxidation; mannitol; protein oxidative modifications; SOD;
D O I
10.1007/BF02784031
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
In the present study the authors report on the enhancing effect of aluminum(III) (Al[III]) on iron(II)(Fe[II])-induced Lipid peroxidation (LPO) of mice brain homogenate, which occurs in a concentration- and time-dependent manner. No evidence of LPO caused by Al alone was found. Both Al(III) and Fe(II) ions induced protein oxidative modifications in mice brain homogenate, in a time-and concentration-dependent manner. Aluminum enhances Fe(II)-induced protein oxidative modification at a concentration of 2:1 and 1:1 Al:Fe molar ratios. However, Al suppress Fe(II)-induced protein oxidative modification at a concentration of 0.5:1 Al:Fe molar ratio. Addition of ethylenediaminetetraacetic acid (EDTA) inhibits both LPO and protein oxidative modifications induced by Al(III) and Fe(II) ions. Addition of mannitol and of superoxide dismutase (SOD) did not show such effects. It is concluded that in mice brain homogenate, Al accelerates Fe(II)-induced LPO. Protein oxidative modifications caused by Fe(II) and/or Al ions are enhanced at high, but suppressed at low concentrations of Al ions. The latter observation suggests a possible biological role of Al as an antioxidant.
引用
收藏
页码:207 / 217
页数:11
相关论文
共 16 条
[1]  
BURGE JA, 1978, METHOD ENZYMOL, V52, P302
[2]   ALUMINUM, NEUROFIBRILLARY DEGENERATION AND ALZHEIMERS DISEASE [J].
CRAPPER, DR ;
KRISHNAN, SS ;
QUITTKAT, S .
BRAIN, 1976, 99 (MAR) :67-80
[3]  
Crapper DR, 1986, NEUROBIOL AGING, V7, P525
[4]   MODIFICATION OF THE BLOOD-BRAIN-BARRIER THROUGH CHRONIC INTOXICATION BY ALUMINUM GLUTAMATE - POSSIBLE ROLE IN THE ETIOLOGY OF ALZHEIMERS-DISEASE [J].
DELONCLE, R ;
GUILLARD, O ;
HUGUET, F ;
CLANET, F .
BIOLOGICAL TRACE ELEMENT RESEARCH, 1995, 47 (1-3) :227-233
[5]   TISSUE SULFHYDRYL GROUPS [J].
ELLMAN, GL .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1959, 82 (01) :70-77
[6]   EFFECTS OF ALUMINUM ON BRAIN LIPID-PEROXIDATION [J].
FRAGA, CG ;
OTEIZA, PI ;
GOLUB, MS ;
GERSHWIN, ME ;
KEEN, CL .
TOXICOLOGY LETTERS, 1990, 51 (02) :213-219
[7]  
HALLIWELL B, 1986, ARCH BIOCHEM BIOPHYS, V246, P510
[8]   ALUMINUM PROMOTES THE AGGREGATION OF ALZHEIMERS AMYLOID BETA-PROTEIN IN-VITRO [J].
KAWAHARA, M ;
MURAMOTO, K ;
KOBAYASHI, K ;
MORI, H ;
KURODA, Y .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 198 (02) :531-535
[9]   AGGREGATION OF AMYLOID BETA-PROTEIN AND ITS NEUROTOXICITY - ENHANCEMENT BY ALUMINUM AND OTHER METALS [J].
KURODA, Y ;
KAWAHARA, M .
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 174 (03) :263-268
[10]  
LOWRY OH, 1951, J BIOL CHEM, V193, P265