Biochemical pathogenesis of post-traumatic epilepsy
Biochemical pathogenesis of post-traumatic epilepsy
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DOI：
10.1007/bf02964604
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发表时间：
1990-04
期刊：
影响因子：
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通讯作者：
A. Mori;M. Hiramatsu;I. Yokoi;R. Edamatsu
中科院分区：
文献类型：
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作者：
A. Mori;M. Hiramatsu;I. Yokoi;R. Edamatsu
头部创伤通常伴随着癫痫，可能与中枢神经系统内的红细胞和血红蛋白的分解有关。已知的是，将血红蛋白或铁盐注射到大鼠的大脑皮质会导致慢性癫痫灶。我们观察了大脑皮层注射三氯化铁后超氧阴离子(O2)和羟基自由基(·OH)的形成，提示这些自由基，特别是·OH，可能与神经细胞膜的脂质过氧化有关，并可能导致脑组织中胍类化合物的加速产生，从而可能导致癫痫的发生。然后，我们发现表没食子儿茶素(EGC)或维生素E和C的磷酸二酯(EPC)是有效的·OH清除剂，显著抑制铁诱导的癫痫灶中丙二醛的形成和癫痫放电。
Head trauma is often followed by epilepsy and may be related to the breakdown of red blood cells and hemoglobin within the CNS. Injection of hemoglobin or iron salts into the rat cortex is known to induce a chronic epileptic focus. We observed the formation of superoxide anion (O2) and hydroxyl radical (·OH) after ferric chloride injection into the rat cerebral cortex and suggest that these radicals, especially ·OH, may be responsible for the initiation of lipid peroxidation in neuronal membranes and for the accelerated production of guanidine compounds in the brain, which may in turn lead to epileptogenicity. Then, we found that treatment with epigallocatechin (EGC) or a phosphate diester of vitamins E and C (EPC), which are potent ·OH scavengers, significantly inhibited the formation of malondialdehyde and epileptic discharges in the iron-induced epileptic focus.