Oxidative stress in schizophrenia: an integrated approach.
Oxidative stress in schizophrenia: an integrated approach.
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DOI：
10.1016/j.neubiorev.2010.10.008
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发表时间：
2011-01
影响因子：
8.2
通讯作者：
Woo, Tsung-Ung W.
中科院分区：
文献类型：
--
作者：
Bitanihirwe, Byron K. Y.;Woo, Tsung-Ung W.
关键词：
氧化应激已被认为有助于精神分裂症的病理生理学。特别是，在精神分裂症中观察到的脂质、蛋白质和DNA的氧化损伤已知会损害细胞活力和功能，这可能随后导致疾病的恶化过程。目前可用的证据指向精神分裂症中酶和非酶抗氧化系统活性的改变。事实上，实验模型已经证明，氧化应激诱导的行为和分子异常与精神分裂症中观察到的异常惊人地相似。这些研究结果表明，氧化应激是密切相关的各种病理生理过程，如炎症，少突胶质细胞异常，线粒体功能障碍，低活性的N-甲基-D-天冬氨酸受体和损伤的快速尖峰γ-氨基丁酸中间神经元。[bkyb 1]这种自我维持机制可能会逐渐恶化，产生与精神分裂症相关的功能和结构后果。最近的临床研究表明，抗氧化剂治疗是有效的改善精神分裂症的症状。因此，确定可行的治疗策略，以解决氧化应激和由此产生的生理紊乱提供了一个令人兴奋的机会，治疗和最终预防精神分裂症。
Oxidative stress has been suggested to contribute to the pathophysiology of schizophrenia. In particular, oxidative damage to lipids, proteins, and DNA as observed in schizophrenia is known to impair cell viability and function, which may subsequently account for the deteriorating course of the illness. Currently available evidence points towards an alteration in the activities of enzymatic and nonenzymatic antioxidant systems in schizophrenia. In fact, experimental models have demonstrated that oxidative stress induces behavioural and molecular anomalies strikingly similar to those observed in schizophrenia. These findings suggest that oxidative stress is intimately linked to a variety of pathophysiological processes, such as inflammation, oligodendrocyte abnormalities, mitochondrial dysfunction, hypoactive N-methyl-D-aspartate receptors and the impairment of fast-spiking gamma-aminobutyric acid interneurons.[bkyb1] Such self-sustaining mechanisms may progressively worsen producing the functional and structural consequences associated with schizophrenia. Recent clinical studies have shown antioxidant treatment to be effective in ameliorating schizophrenic symptoms. Hence, identifying viable therapeutic strategies to tackle oxidative stress and the resulting physiological disturbances provide an exciting opportunity for the treatment and ultimately prevention of schizophrenia.
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影响因子：
10.6
作者：
ADLER, LE;HOFFER, LJ;FREEDMAN, R
通讯作者：
FREEDMAN, R
影响因子：
4.4
作者：
Bitanihirwe, B. K. Y.;Lim, M. P.;Woo, T. U. W.
通讯作者：
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作者：
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通讯作者：
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作者：
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