Exacerbation of Delayed Cell Injury After Transient Global Ischemia in Mutant Mice With CuZn Superoxide Dismutase Deficiency | Zendy

Makoto Kawase | Zendy; Kensuke Murakami | Zendy; Miki Fujimura | Zendy; Yuiko MoritaFujimura | Zendy; Yvan Gasche | Zendy; Takeo Kondo | Zendy; Richard Scott | Zendy; Pak H. Chan | Zendy

Open Access

Exacerbation of Delayed Cell Injury After Transient Global Ischemia in Mutant Mice With CuZn Superoxide Dismutase Deficiency

Author(s) -

Makoto Kawase,

Kensuke Murakami,

Miki Fujimura,

Yuiko MoritaFujimura,

Yvan Gasche,

Takeo Kondo,

Richard Scott,

Pak H. Chan

Publication year - 1999

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/01.str.30.9.1962

Subject(s) - superoxide dismutase , superoxide , ischemia , medicine , pathogenesis , endocrinology , brain ischemia , hippocampal formation , oxidative stress , biology , biochemistry , enzyme

We have demonstrated that copper-zinc superoxide dismutase (CuZn-SOD), a cytosolic isoenzyme of SODs, has a protective role in the pathogenesis of superoxide radical-mediated brain injury. Using mice bearing a disruption of the CuZn-SOD gene (Sod1), the present study was designed to clarify the role of superoxide anion in the pathogenesis of selective vulnerability after transient global ischemia.

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