Age dependence of seizure-induced oxidative stress
Age dependence of seizure-induced oxidative stress
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DOI：
10.1016/s0306-4522(02)00979-x
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发表时间：
2003-01-01
期刊：
影响因子：
3.3
通讯作者：
Li, QY
中科院分区：
文献类型：
--
作者：
Patel, M;Li, QY
未成熟大脑对脑损伤诱导的神经元死亡的脆弱性降低的机制仍然未知。我们询问氧化应激是否在未成熟动物对麻醉诱导的脑损伤的抵抗中起作用。线粒体顺乌头酸酶失活和8-羟基-2-脱氧鸟苷（8-OHdG）分别被用作稳态线粒体超氧阴离子（O-2（-））产生和氧化DNA损伤的指标，红藻氨酸诱导的癫痫发作导致成年大鼠（出生后30天或以上）线粒体顺乌头酸酶失活和8-OHdG形成增加，但未成年大鼠（出生后12和21天）则没有。红藻氨酸管理没有诱导锰超氧化物歧化酶（MnSOD）或CuZnSOD在未成年或成年大鼠。红藻氨酸盐癫痫发作后线粒体O-2（-）产生和氧化DNA损伤的发育增加表明，线粒体氧化应激可能是使发育中的大脑对癫痫诱导的脑损伤具有抵抗力的关键因素。(C)2003年由Elsevier Science Ltd代表IBRO出版。
The mechanisms underlying the decreased vulnerability of the immature brain to seizure-induced neuronal death remain unknown. We asked whether oxidative stress plays a role in the resistance of immature animals to seizure-induced brain damage. Mitochondrial aconitase inactivation and 8-hydroxy-2-deoxyguanosine (8-OHdG) were used as indices of steady-state mitochondrial superoxide (O-2(-)) production and oxidative DNA damage, respectively.Kainate-induced seizures resulted in increased mitochondrial aconitase inactivation and 8-OHdG formation in adult (postnatal day 30 or more), but not in immature rats (postnatal days 12 and 21). Kainate administration did not induce manganese superoxide dismutase (MnSOD) or CuZnSOD in immature or adult rats. This developmental increase in mitochondrial O-2(-) production and oxidative DNA damage following kainate seizures suggests that mitochondrial oxidative stress may be a key factor that renders the developing brain resistant to seizure-induced brain damage. (C) 2003 Published by Elsevier Science Ltd on behalf of IBRO.