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

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。
批准号:
04454362
负责人:
MORI Akitane
金额:
$3.58万
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
项目状态:
已结题
起止时间:
1992 至 1994

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中文摘要
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英文摘要
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.
期刊论文(62)
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会议论文
Mori A,Hiramatsu M and Yokoi I: "Free Radicals in the Brain Aging, Neurobiological and Mental Disorders" Springer-Verlag,Berlin, 14 (1994)
Mori A、Hiramatsu M 和 Yokoi I:“大脑老化、神经生物学和精神疾病中的自由基”Springer-Verlag,柏林,14 (1994)
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Mori A,Yokoi I,Liu J and Mizukawa K: "Oxidative Stress and Aging" Birkhauser Verl., Basel(in press), (1995)
Mori A、Yokoi I、Liu J 和 Mizukawa K:“氧化应激与衰老”Birkhauser Verl.,巴塞尔(出版中),(1995 年)
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Kabuto H,Yokoi I,and Mori A: "Monoamine metabolites, iron induced seizures, and the anticonvulsant effect of tannis." Neurochem.Res.17. 585-590 (1992)
Kabuto H、Yokoi I 和 Mori A:“单胺代谢物、铁诱导的癫痫发作以及丹宁酸的抗惊厥作用。”
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羽部仁: "マウス脳内窒素酸化物量の検討" Neurosciences. 19. 165-168 (1993)
Hitoshi Habe:“小鼠大脑中一氧化氮含量的研究”《神经科学》19. 165-168 (1993)。
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29
    El mice : Seizure mechanisms and their management
    • 批准号:
      02304045
    • 项目类别:
      Grant-in-Aid for Co-operative Research (A)
    • 资助金额:
      $1.92万
    • 财政年份:
      1990
    • 负责人:
      MORI Akitane
    • 依托单位:
    Neurochemical and neurophysiological mechanism for guanidino compoundinduced seizures
    • 批准号:
      58440081
    • 项目类别:
      Grant-in-Aid for General Scientific Research (A)
    • 资助金额:
      $10.05万
    • 财政年份:
      1983
    • 负责人:
      MORI Akitane
    • 依托单位: