Human copper-zinc superoxide dismutase transgenic mice are highly resistant to reperfusion injury after focal cerebral ischemia. | Zendy

GuoYuan Yang | Zendy; Pak H. Chan | Zendy; J Chen | Zendy; E. Carlson | Zendy; S F Chen | Zendy; Philip R. Weinstein | Zendy; C. J. Epstein | Zendy; Hideyuki Kamii | Zendy

Open Access

Human copper-zinc superoxide dismutase transgenic mice are highly resistant to reperfusion injury after focal cerebral ischemia.

Author(s) -

GuoYuan Yang,

Pak H. Chan,

J Chen,

E. Carlson,

S F Chen,

Philip R. Weinstein,

C. J. Epstein,

Hideyuki Kamii

Publication year - 1994

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.25.1.165

Subject(s) - medicine , superoxide dismutase , ischemia , reperfusion injury , genetically modified mouse , zinc , transgene , stroke (engine) , dismutase , copper , pathology , oxidative stress , biochemistry , gene , biology , mechanical engineering , materials science , chemistry , organic chemistry , engineering , metallurgy

We have demonstrated in a previous study that superoxide radicals play a role in the pathogenesis of cerebral infarction, using a transgenic mouse model of distal middle cerebral artery occlusion, permanent ipsilateral cerebral carotid artery occlusion, and 1-hour contralateral cerebral carotid artery occlusion that produced infarction only in the cortex. However, the role of superoxide radicals in reperfusion injury in transgenic mice overexpressing superoxide dismutase (SOD) is unknown. Using a mouse model of intraluminal blockade of middle cerebral artery that produced both cortical and striatal infarction, we now further examined the role of superoxide radicals in ischemic cerebral infarction after reperfusion in transgenic mice overexpressing human CuZn-SOD activity.

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