Neonatal iron exposure induces oxidative stress in adult Wistar rat

被引:50
作者
Dal-Pizzol, F
Klamt, F
Frota, MLC
Andrades, ME
Caregnato, FF
Vianna, MMR
Schröder, N
Quevedo, J
Izquierdo, I
Archer, T
Moreira, JCF
机构
[1] Univ Fed Rio Grande do Sul, Inst Ciencias Basicas Saude, Dept Bioquim, Lab Estresse Oxidativo, BR-90035003 Porto Alegre, RS, Brazil
[2] Univ Extremo Sul Catarinese, Dept Med, BR-88806000 Criciuma, SC, Brazil
[3] Univ Luterana Brasil, Ctr Integrado Canc, CINCAN, Canoas, RS, Brazil
[4] Univ Fed Rio Grande do Sul, Inst Ciencias Basicas Saude, Dept Bioquim, Ctr Memoria, BR-90035003 Porto Alegre, RS, Brazil
[5] Univ Gothenburg, Dept Psychol, Gothenburg, Sweden
来源
DEVELOPMENTAL BRAIN RESEARCH | 2001年 / 130卷 / 01期
关键词
iron supplementation; neonatal; oxidative stress; superoxide dismutase; TBARS; protein carbonyl; Parkinson's disease;
D O I
10.1016/S0165-3806(01)00218-8
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Oxidative stress and excess of iron in the brain has been implicated in a variety of acute and chronic neurological conditions. The neonatal period is critical for the establishment of normal iron content in the adult brain. In the present study, the long-term oxidative effects of iron exposure during this period were assessed by treating Wistar rats orally with 0, 7.5 or 15 mg Fe+2/kg of body weight on postnatal days 10-12. Thiobarbituric acid reactive species, protein carbonyl, superoxide dismutase activity were measured at the age of 3 months. It was found that there was an increase in thiobarbituric acid reactive species and protein carbonyl in the substantia nigra of iron treated rats. In contrast, oxidative stress in the striatum was decreased. Superoxide dismutase activity was decreased in the substantia nigra iron treated rats. There were no differences in cerebellum measures among the groups. Our results demonstrated that iron supplementation in a critical neonatal period induced oxidative stress and modulated SOD activity in the adult life in selective brain regions. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:109 / 114
页数:6
相关论文
共 37 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   OXIDANTS, ANTIOXIDANTS, AND THE DEGENERATIVE DISEASES OF AGING [J].
AMES, BN ;
SHIGENAGA, MK ;
HAGEN, TM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :7915-7922
[3]   Attenuation of 6-hydroxydopamine-induced dopaminergic nigrostriatal lesions in superoxide dismutase transgenic mice [J].
Asanuma, M ;
Hirata, H ;
Cadet, JL .
NEUROSCIENCE, 1998, 85 (03) :907-917
[4]  
Bannister J. V, 1987, METHOD BIOCHEM ANAL, P279
[5]   Mitochondrial free radical generation, oxidative stress, and aging [J].
Cadenas, E ;
Davies, KJA .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (3-4) :222-230
[6]   A HISTOCHEMICAL-STUDY OF IRON-POSITIVE CELLS IN THE DEVELOPING RAT-BRAIN [J].
CONNOR, JR ;
PAVLICK, G ;
KARLI, D ;
MENZIES, SL ;
PALMER, C .
JOURNAL OF COMPARATIVE NEUROLOGY, 1995, 355 (01) :111-123
[7]   Retinol supplementation induces DNA damage and modulates iron turnover in rat Sertoli cells [J].
Dal-Pizzol, F ;
Klamt, F ;
Frota, MLC ;
Moraes, LF ;
Cláudio, J ;
Moreira, F ;
Benfato, MS .
FREE RADICAL RESEARCH, 2000, 33 (05) :677-687
[8]   Lipid peroxidation in hippocampus early and late after status epilepticus induced by pilocarpine or kainic acid in Wistar rats [J].
Dal-Pizzol, F ;
Klamt, F ;
Vianna, MMR ;
Schröder, N ;
Quevedo, J ;
Benfato, MS ;
Moreira, JCF ;
Walz, R .
NEUROSCIENCE LETTERS, 2000, 291 (03) :179-182
[9]   OXIDATIVELY DENATURED PROTEINS ARE DEGRADED BY AN ATP-INDEPENDENT PROTEOLYTIC PATHWAY IN ESCHERICHIA-COLI [J].
DAVIES, KJA ;
LIN, SW .
FREE RADICAL BIOLOGY AND MEDICINE, 1988, 5 (04) :225-236
[10]  
DEXTER DT, 1987, LANCET, V2, P1219