ANTIOXIDANT ENZYMES IN THE BRAIN OF ZITTER RATS - ABNORMAL-METABOLISM OF OXYGEN SPECIES AND ITS RELEVANCE TO PATHOGENIC CHANGES IN THE BRAIN OF ZITTER RATS WITH GENETIC SPONGIFORM ENCEPHALOPATHY
ANTIOXIDANT ENZYMES IN THE BRAIN OF ZITTER RATS - ABNORMAL-METABOLISM OF OXYGEN SPECIES AND ITS RELEVANCE TO PATHOGENIC CHANGES IN THE BRAIN OF ZITTER RATS WITH GENETIC SPONGIFORM ENCEPHALOPATHY
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DOI：
10.1016/0006-8993(94)90373-5
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发表时间：
1994-08-08
期刊：
影响因子：
2.9
通讯作者：
YAMANOUCHI, K
中科院分区：
文献类型：
--
作者：
GOMI, H;UENO, I;YAMANOUCHI, K
Zitter大鼠发展为遗传性海绵状脑病，其特征是大脑发生水肿变化。为了阐明活性氧在这一过程中的作用，我们研究了代谢活性氧的酶活性的年龄相关变化。比较了zitter大鼠脑和肝脏超氧化物歧化酶（SOD）、d -氨基酸氧化酶（D-AAO）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶的活性。在退行性变的成年zitter大鼠脑内，SOD和D-AAO活性明显增强，过氧化氢酶活性低于SD/J大鼠。在乳腺炎大鼠脑空泡形成之前或同时，过氧化氢酶和D-AAO明显异常，而SOD活性不明显。zitter和SD/J大鼠脑内GSH-Px活性无差异。这些结果表明，过氧化氢（H2O2）代谢在微过氧化物酶体中的改变可能在zitter大鼠大脑退行性变化的起始中起重要作用。成年zitter大鼠脑内SOD活性的增强可能是对H2O2停滞引起的细胞损伤过程中产生的高超氧阴离子的代偿反应。同时，更多的SOD可能产生更多的H2O2。
Zitter rats develop a genetic spongiform encephalopathy characterized by edematous changes in their brains. In order to elucidate the involvement of reactive oxygen species in this process we examined age-related alterations of the activities of the enzymes which metabolize reactive oxygen species. Activities of superoxide dismutase (SOD), D-amino acid oxidase (D-AAO), glutathione peroxidase (GSH-Px) and catalase in the brain and the liver of zitter rats are compared with those of control SD/J rats. In the brain of adult zitter rats which show degenerative changes, significantly enhanced activities of SOD and D-AAO were obtained, whereas activity of catalase was lower than that of the SD/J rats. Prominent abnormalities in catalase and D-AAO but not in SOD activity were demonstrated before or at the same time as the appearance of the morphological vacuolation in the brain of suckling zitter rats. There was no difference in GSH-Px activity between the brains from zitter and SD/J rats. These results suggest that the alteration of hydrogen peroxide (H2O2)-metabolism in microperoxisomes may play an important role in the initiation of degenerative changes in the brain of zitter rats. Enhanced SOD activity observed in the brain of adult zitter rats may be a compensatory response to the high superoxide anion produced in the course of cell damage caused by the H2O2 stagnation. Also, more SOD might produce more H2O2.