Comparative analysis of superoxide dismutase activity between acute pharmacological models and a transgenic mouse model of Huntington's disease

被引:50
作者
Santamaría, A
Pérez-Severiano, F
Rodríguez-Martínez, E
Maldonado, PD
Pedraza-Chaverri, J
Ríos, C
Segovia, J
机构
[1] IPN, Ctr Invest & Estudios Avanzados, Dept Fisiol Biofis & Neurociencias, Mexico City 07300, DF, Mexico
[2] SSA, Inst Nacl Neurol & Neurocirugia Manuel Velasco Su, Dept Neuroquim, Mexico City 14629, DF, Mexico
[3] Univ Nacl Autonoma Mexico, Fac Quim, Mexico City 04510, DF, Mexico
关键词
striatum; oxidative damage; free radicals; excitotoxins; transgenic; Huntington's disease; superoxide dismutase;
D O I
10.1023/A:1010911417383
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
We examined the activity of striatal superoxide dismutase (SOD) in two acute pharmacological models of Huntington's disease (HD), and compared it with SOD activity in the striata of mice transgenic for the HD mutation. Total SOD, and Cu/ZnSOD activities increased in young transgenic mice, but decreased in older (35 week) mice. We consider that the increased enzyme. activity represents a compensatory mechanism to protect cells from free radical-induced damage, but the system becomes insufficient in older animals. Major decreases in SOD activity were also observed both after quinolinic acid and 3-nitropropionic acid intrastriatal injections. The present results indicate that in both types of HD models striatal oxidative damage occurs, and that it is associated with alterations in the cellular antioxidant system.
引用
收藏
页码:419 / 424
页数:6
相关论文
共 27 条
  • [1] BEAL MF, 1991, J NEUROSCI, V11, P1649
  • [2] REPLICATION OF THE NEUROCHEMICAL CHARACTERISTICS OF HUNTINGTONS-DISEASE BY QUINOLINIC ACID
    BEAL, MF
    KOWALL, NW
    ELLISON, DW
    MAZUREK, MF
    SWARTZ, KJ
    MARTIN, JB
    [J]. NATURE, 1986, 321 (6066) : 168 - 171
  • [3] Mitochondrial Dysfunction in Neurodegenerative Diseases
    Johri, Ashu
    Beal, M. Flint
    [J]. JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2012, 342 (03) : 619 - 630
  • [4] AGE-DEPENDENT VULNERABILITY OF THE STRIATUM TO THE MITOCHONDRIAL TOXIN 3-NITROPROPIONIC ACID
    BROUILLET, E
    JENKINS, BG
    HYMAN, BT
    FERRANTE, RJ
    KOWALL, NW
    SRIVASTAVA, R
    ROY, DS
    ROSEN, BR
    BEAL, MF
    [J]. JOURNAL OF NEUROCHEMISTRY, 1993, 60 (01) : 356 - 359
  • [5] Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease
    Chen, M
    Ona, VO
    Li, MW
    Ferrante, RJ
    Fink, KB
    Zhu, S
    Bian, J
    Guo, L
    Farrell, LA
    Hersch, SM
    Hobbs, W
    Vonsattel, JP
    Cha, JHJ
    Friedlander, RM
    [J]. NATURE MEDICINE, 2000, 6 (07) : 797 - +
  • [6] LESION OF STRIATAL NEURONS WITH KAINIC ACID PROVIDES A MODEL FOR HUNTINGTONS-CHOREA
    COYLE, JT
    SCHWARCZ, R
    [J]. NATURE, 1976, 263 (5574) : 244 - 246
  • [7] Transgenic mice expressing a Huntington's disease mutation are resistant to quinolinic acid-induced striatal excitotoxicity
    Hansson, O
    Petersén, Å
    Leist, M
    Nicotera, P
    Castilho, RF
    Brundin, P
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (15) : 8727 - 8732
  • [8] HARPER PS, 1906, HUNTINGTON DIS, P123
  • [9] A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration
    Hodgson, JG
    Agopyan, N
    Gutekunst, CA
    Leavitt, BR
    LePiane, F
    Singaraja, R
    Smith, DJ
    Bissada, N
    McCutcheon, K
    Nasir, J
    Jamot, L
    Li, XJ
    Stevens, ME
    Rosemond, E
    Roder, JC
    Phillips, AG
    Rubin, EM
    Hersch, SM
    Hayden, MR
    [J]. NEURON, 1999, 23 (01) : 181 - 192
  • [10] USE OF CYANIDE AND DIETHYLDITHIOCARBAMATE IN THE ASSAY OF SUPEROXIDE DISMUTASES
    IQBAL, J
    WHITNEY, P
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1991, 10 (01) : 69 - 77