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Reactive oxygen species are involved in the mechanism of epileptogenic focus formation after head injury.

活性氧参与头部损伤后致癫痫病灶形成的机制。

基本信息

批准号：
04454362
负责人：
MORI Akitane
金额：
$ 3.58万
依托单位：
Okayama University Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1994
项目状态：
已结题

项目摘要

1. The normal brain was found to scavenge both superoxide (O^-_2) and hydroxyl radicals (・OH) . However brain damage can be induced by excess reactive oxygen species (ROS) since they are known to react virtually with any type of molecule such as nucleic acid, membran lipids, and protein in the brian, and may result in an epileptogenic focus formation.2. An injection of iron ion into the rat brain decreased nitric oxide (NO) from arginine by nitric oxide synthase (NOS). Generally, No is thougt to play an inhibitory role in the seizure mechanism. Therefore, decreased NO may accelerate the seizure procedure induced by iron ion. alpha-Guanidinoglutaric acid, an endogenous convulsant, could induced seizures by inhibiting NOS activity.3. Oxygen inhalation for 3 weeks accelerated the formation of ・OH,・ R and methylguanidine, an endogenous convulsant. We proposed that oxygen inhalation is a clinical first aid for patients with severe head injury, but the clinical beneficial concentration and period for treatment should be reexamined carefully from the veiw point of oxygen intoxication.4. Superoxide dismutase (SOD) was induced in the iron induced epileptogenic focus in the rat brian. It may be a defense mechanism against excess O^-_2 induced by iron ion in the brian.5. Antioxidants or free radical scavengers, e.g., epigallocatechin and its derivatives, adenosine and chlor-adenosin could be a possible rational treatment for post-traumatic epilepsy. As well, probcol, TJ960 (a Japanese herbal medicine) , baicalein (an effective component of TJ960) , and Bio-normalizer (a natural healthy food) may be effective for it, as they are found to be effective free radical scavengers.

1.正常脑组织中同时存在超氧阴离子（O^-2）和羟自由基（·OH）。然而，过量的活性氧（ROS）可以引起脑损伤，因为已知它们几乎可以与脑中的任何类型的分子如核酸、膜脂质和蛋白质反应，并可能导致癫痫灶形成。大鼠脑内注射铁离子可减少一氧化氮合酶（NOS）从精氨酸中释放一氧化氮（NO）。一般认为NO在癫痫发作机制中起抑制作用。因此，NO减少可能加速铁离子诱发的癫痫发作过程。内源性惊厥剂α-胍基谷氨酸可通过抑制NOS活性诱发癫痫发作.吸氧3周可促进内源性惊厥剂·OH、· R和甲基胍的生成。提出吸氧是重型颅脑损伤患者的临床急救措施，但应从氧中毒的角度重新审视临床有益浓度和治疗时间.用铁致痫大鼠脑内超氧化物歧化酶（SOD）活性。这可能是铁离子诱导的鳃对过量O^-2的一种防御机制.抗氧化剂或自由基清除剂，例如，表没食子儿茶素及其衍生物、腺苷和氯腺苷可能是治疗外伤后癫痫的一种合理药物。此外，probcol，TJ 960（日本草药），黄芩素（TJ 960的有效成分）和Bio-normalizer（天然健康食品）可能对其有效，因为它们被发现是有效的自由基清除剂。