Increased oxidative damage to DNA in a transgenic mouse model of Huntington's disease

被引：197
|
作者：
Bogdanov, MB
Andreassen, OA
Dedeoglu, A
Ferrante, RJ
Beal, MF
机构：
[1] Massachusetts Gen Hosp, Neurol Serv, Neurochem Lab, Boston, MA 02114 USA
[2] Harvard Univ, Sch Med, Boston, MA USA
[3] Vet Adm Med Ctr, Ctr Geriatr Res Educ & Clin, Bedford, MA USA
[4] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA
[5] Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA
[6] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA
[7] New York Presbyterian Hosp, New York, NY USA
来源：
JOURNAL OF NEUROCHEMISTRY | 2001年 / 79卷 / 06期
关键词：
free radicals; Huntington's disease; 8-hydroxy-2-deoxyguanosine; oxidative damage; microdialysis; transgenic;
D O I：
10.1046/j.1471-4159.2001.00689.x
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：
Mitochondrial dysfunction and oxidative damage may play a role in the pathogenesis of Huntington's disease (HD). We examined concentrations of 8-hydroxy-2-deoxyguanosine (OH(8)dG), a well-established marker of oxidative damage to DNA, in a transgenic mouse model of HD (R6/2). Increased concentrations of OH(8)dG were found in the urine, plasma and striatal microdialysates of the HD mice. Increased concentrations were also observed in isolated brain DNA at 12 and 14 weeks of age. Immunocytochemistry showed increased OH(8)dG staining in late stages of the illness. These results suggest that oxidative damage may play a role in the pathogenesis of neuronal degeneration in the R6/2 transgenic mouse model of HD.
引用
收藏
页码：1246 / 1249
页数：4
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