Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology, Zurich, Schorenstrasse 16, Schwerzenbach CH 8603, Switzerland.
Neurosci Biobehav Rev. 2011 Jan;35(3):878-93. doi: 10.1016/j.neubiorev.2010.10.008. Epub 2010 Oct 23.
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 behavioral 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. 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.
氧化应激被认为与精神分裂症的病理生理学有关。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。目前的证据表明，精神分裂症中酶和非酶抗氧化系统的活性发生了改变。事实上，实验模型表明，氧化应激会导致行为和分子异常，与精神分裂症中观察到的异常非常相似。这些发现表明，氧化应激与多种病理生理过程密切相关，如炎症、少突胶质细胞异常、线粒体功能障碍、N-甲基-D-天冬氨酸受体活性降低以及快速放电 γ-氨基丁酸中间神经元功能障碍。这种自我维持的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，抗氧化治疗在改善精神分裂症症状方面是有效的。因此，确定可行的治疗策略来应对氧化应激和由此产生的生理紊乱，为治疗和最终预防精神分裂症提供了一个令人兴奋的机会。
