While neurotransmitter dysfunction represents a key component in mental illnesses, there is now a wide agreement for a central pathophysiological hub that includes hormones, neuroinflammation, redox mechanisms as well as oxidative stress. With respect to oxidation-reduction (redox) mechanisms, preclinical and clinical evidence suggests that an imbalance in the pro/anti-oxidative homeostasis toward the increased production of substances with oxidizing potential may contribute to the etiology and manifestation of different psychiatric disorders. The substantial and continous demand for energy renders the brain highly susceptible to disturbances in its energy supply, especially following exposure to stressful events, which may lead to overproduction of reactive oxygen and nitrogen species under conditions of perturbed antioxidant defenses. This will eventually induce different molecular alterations, including extensive protein and lipid peroxidation, increased blood-brain barrier permeability and neuroinflammation, which may contribute to the changes in brain function and morphology observed in mental illnesses. This view may also reconcile different key concepts for psychiatric disorders, such as the neurodevelopmental origin of these diseases, as well as the vulnerability of selective cellular populations that are critical for specific functional abnormalities. The possibility to pharmacologically modulate the redox system is receiving increasing interest as a novel therapeutic strategy to counteract the detrimental effects of the unbalance in brain oxidative mechanisms. This review will describe the main mechanisms and mediators of the redox system and will examine the alterations of oxidative stress found in animal models of psychiatric disorders as well as in patients suffering from mental illnesses, such as schizophrenia and major depressive disorder. In addition, it will discuss studies that examined the effects of psychotropic drugs, including antipsychotics and antidepressants, on the oxidative balance as well as studies that investigated the effectiveness of a direct modulation of oxidative mechanisms in counteracting the behavioral and functional alterations associated with psychiatric disorders, which supports the promising role of the redox system as a novel therapeutic target for the improved treatment of brain disorders.

中文翻译：

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精神疾病中的氧化还原机制：药理干预的新目标。

虽然神经递质功能障碍是精神疾病的关键组成部分，但现在人们已经广泛同意建立一个包括激素，神经炎症，氧化还原机制以及氧化应激在内的中央病理生理枢纽。关于氧化还原（redox）机理，临床前和临床证据表明，前/抗氧化稳态的不平衡会增加具有氧化潜力的物质的产生，这可能会导致不同精神疾病的病因和表现。对能量的大量且持续的需求使大脑高度容易受到能量供应的干扰，尤其是在暴露于压力事件之后，这可能会在抗氧化防御措施受到干扰的情况下导致活性氧和氮物种的过量生产。这最终将导致不同的分子改变，包括广泛的蛋白质和脂质过氧化作用，血脑屏障通透性增加和神经炎症，这可能导致精神疾病中观察到的脑功能和形态改变。这种观点还可能调和精神疾病的不同关键概念，例如这些疾病的神经发育起源，以及对于特定功能异常至关重要的选择性细胞群体的脆弱性。药理学上调节氧化还原系统的可能性作为一种新的治疗策略来抵消脑氧化机制不平衡的有害影响，引起了越来越多的关注。这篇综述将描述氧化还原系统的主要机制和介质，并研究在精神疾病的动物模型以及患有精神疾病（例如精神分裂症和重度抑郁症）的患者中发现的氧化应激变化。此外，还将讨论检查包括抗精神病药和抗抑郁药在内的精神药物对氧化平衡的影响的研究，以及研究直接调节氧化机制在抵消与精神疾病相关的行为和功能改变方面的有效性的研究。 ，它支持氧化还原系统作为改善脑部疾病的新型治疗靶标的有希望的作用。