Oxidative stress is attenuated in mice overexpressing BCL-2

被引：57

作者：

Bogdanov, MB

Ferrante, RJ

Mueller, G

Ramos, LE

Martinou, JC

Beal, MF ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Neurol Serv, Neurochem Lab, Boston, MA 02114 USA

[2] Harvard Univ, Sch Med, Boston, MA 02114 USA

[3] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA

[4] Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA

[5] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA

[6] Dept Vet Affairs, Bedford, MA USA

[7] Glaxo Inst Mol Biol SA, CH-1228 Geneva, Switzerland

[8] Cornell Univ, Med Ctr, New York Hosp, Dept Neurol, New York, NY 10021 USA

来源：

NEUROSCIENCE LETTERS | 1999年 / 262卷 / 01期

关键词：

oxidative stress; Bcl-2; mitochondria; apoptosis; 3-nitropropionic acid; Huntington's disease;

D O I：

10.1016/S0304-3940(99)00047-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The protooncogene Bcl-2 inhibits apoptosis in neural cells, which may involve mitochondrial stabilization and decreased generation of reactive oxygen species. Using in vivo microdialysis we found that following administration of the mitochondrial toxin 3-nitropropionic acid (3-NP) there was a significant increase in the conversion of 4-hydroxybenzoic acid (4-HBA) to 3,4-dihydroxybenzoic acid (3,4-DHBA) in control mice, but not in Bcl-2 overexpressing mice. Striatal lesions were observed in littermate control mice, whereas, lesions were minimal or absent in Bcl-2 overexpressing mice. This shows that Bcl-2 overexpression in vivo attenuates the generation of reactive oxygen species. (C) 1999 Published by Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：33 / 36

页数：4

共 30 条

[1]

BAFFY G, 1993, J BIOL CHEM, V268, P6511

[2]

BEAL MF, 1995, J NEUROCHEM, V65, P919

[3]

BEAL MF, 1993, J NEUROSCI, V13, P4181

[4] Neural apoptosis [J].