Early and transient increase in oxidative stress in the cerebral cortex of senescence-accelerated mouse
Early and transient increase in oxidative stress in the cerebral cortex of senescence-accelerated mouse
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DOI：
10.1016/0047-6374(95)01681-3
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发表时间：
1996-02-24
影响因子：
5.3
通讯作者：
Ishibashi, S
中科院分区：
文献类型：
--
作者：
Sato, E;Oda, N;Ishibashi, S
研究了加速衰老小鼠（SAM）的一个亚系SAMP 8与SAMR 1大脑皮层中氧化应激的变化，SAMR 1用作对照。过氧化脂质和蛋白质羰基含量在4- 8周龄的SAMP 8中短暂增加。过氧化脂质的增加仅见于大脑皮层，而大脑的其他区域未出现。此外，在SAMP 8中，脑细胞中活性氧簇的净产生也增加。此外，在SAMP 8的大脑皮层中，谷氨酰胺合成酶（已知为对活性氧高度敏感的酶）的活性从4周龄至8周龄降低。这些结果表明，氧化应激可能是诱导在大脑皮层的SAMP 8从4- 8周龄，在SAMP 8的大脑中的独特的缺陷的外观之前。
Age-related changes in oxidative stress in the cerebral cortex of SAMP8, a substrain of senescence-accelerated mouse (SAM), were investigated in comparison with those in SAMR1, which were used as a control. The lipid peroxide and protein carbonyl contents were transiently increased in SAMP8 from 4- to 8-weeks of age. The increases in lipid peroxide were seen only in the cerebral cortex and not in other regions of the cerebrum. Furthermore, the net generation of reactive oxygen species in cerebral cells was also increased in SAMP8. In addition, the activity of glutamine synthetase, which is known as an enzyme highly sensitive to reactive oxygen, was decreased in the cerebral cortex of SAMP8 from 4- to 8-weeks of age. These results suggest that oxidative stress may be induced in the cerebral cortex of SAMP8 from 4- to 8-weeks of age, preceding the appearance of distinctive deficits in the brain of SAMP8.