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氧自由基与脑功能障碍。

Oxygen free radicals and brain dysfunction.

作者信息

Jesberger J A, Richardson J S

机构信息

Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.

出版信息

Int J Neurosci. 1991 Mar;57(1-2):1-17. doi: 10.3109/00207459109150342.

Abstract

Oxygen free radicals, any chemical moiety containing an oxygen atom with an unpaired electron in the outer orbital shell, are generated during many normal biochemical reactions in living tissue. The unpaired electron makes these compounds highly reactive and they can initiate disruptive peroxidation reactions with various substrates important to the survival of cells such as proteins, lipids and nucleic acids. A fairly complex defense system has evolved to protect living tissue from free radicals and to minimize the damage they might cause. Neurons are especially vulnerable to free radical attack and impaired defenses or exposure to excess free radicals can lead to neuronal death. Free radicals contribute to neuronal loss in cerebral ischemia and hemorrhage and may be involved in the degeneration of neurons in epilepsy, schizophrenia, tardive dyskinesia, normal aging, Parkinson's Disease and Alzheimer's Disease. The development of drugs that limit or prevent the attack of free radicals on neurons would be an important advance in the treatment of these conditions.

摘要

氧自由基是指任何在外层轨道壳中含有一个未配对电子的氧原子的化学基团,它们在活组织的许多正常生化反应过程中产生。未配对电子使这些化合物具有高度反应性,并且它们能够与对细胞存活至关重要的各种底物(如蛋白质、脂质和核酸)引发破坏性的过氧化反应。已经进化出一个相当复杂的防御系统来保护活组织免受自由基的侵害,并将它们可能造成的损害降至最低。神经元特别容易受到自由基攻击,防御功能受损或暴露于过量自由基会导致神经元死亡。自由基导致脑缺血和出血中的神经元损失,并且可能参与癫痫、精神分裂症、迟发性运动障碍、正常衰老、帕金森病和阿尔茨海默病中神经元的退化。开发限制或防止自由基对神经元攻击的药物将是这些病症治疗中的一项重要进展。

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