Superoxide production and the activity of MnSOD in rat brain after intrahippocampal kainate-induced seizure

L. Radenović, M. Jovanović, I. Vasiljević, V. Selaković
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引用次数: 3

Abstract

Glutamate neurotoxicity has been hypothesized to underlie several types of acute brain injury. Free radical reactions are implicated in a variety of physiological and pathological processes and abnormalities associated with superoxide dismutase (SOD) have been recently documented in several neurodegenerative processes. We investigated superoxide production and MnSOD activity after kainate injection into the CA3 region of the rat hippocampus. The measurements take place at different times in the hippocampus, forebrain cortex, straitum and cerebellum homogenates. Free radicals including superoxide are responsible for postlesional cytotoxicity. The increase of MnSOD in distinct brain regions, which are functionally connected via afferents and efferents, suggests that these regions are affected by the injury. It suggests that MnSOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity.
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海马内盐诱导癫痫发作后大鼠脑内超氧化物产生及MnSOD活性的研究
谷氨酸神经毒性已被假设为几种类型的急性脑损伤的基础。自由基反应涉及多种生理和病理过程,超氧化物歧化酶(SOD)异常最近在几种神经退行性过程中得到证实。我们研究了海盐酸盐注入大鼠海马CA3区后超氧化物的产生和MnSOD的活性。海马、前脑皮层、海马状突起和小脑匀质在不同时间进行测量。包括超氧化物在内的自由基是造成病变后细胞毒性的原因。MnSOD在通过传入和传出功能连接的不同脑区增加,表明这些区域受到损伤的影响。这表明MnSOD保护这些区域的细胞免受超氧化物诱导的损伤,因此可能限制神经毒性的逆行和顺行扩散。
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