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精神分裂症患者的加速衰老:氧化应激的潜在作用。

Accelerated aging in schizophrenia patients: the potential role of oxidative stress.

机构信息

Department of Psychiatry and Behavioral Sciences, the University of Texas Health Science Center at Houston, Texas, USA.

出版信息

Aging Dis. 2013 Dec 4;5(4):256-62. doi: 10.14336/AD.2014.0500256. eCollection 2014 Aug.

Abstract

Several lines of evidence suggest that schizophrenia, a severe mental illness characterized by delusions, hallucinations and thought disorder is associated with accelerated aging. The free radical (oxidative stress) theory of aging assumes that aging occurs as a result of damage to cell constituents and connective tissues by free radicals arising from oxygen-associated reactions. Schizophrenia has been associated with oxidative stress and chronic inflammation, both of which also appear to reciprocally induce each other in a positive feedback manner. The buildup of damaged macromolecules due to increased oxidative stress and failure of protein repair and maintenance systems is an indicator of aging both at the cellular and organismal level. When compared with age-matched healthy controls, schizophrenia patients have higher levels of markers of oxidative cellular damage such as protein carbonyls, products of lipid peroxidation and DNA hydroxylation. Potential confounders such as antipsychotic medication, smoking, socio-economic status and unhealthy lifestyle make it impossible to solely attribute the earlier onset of aging-related changes or oxidative stress to having a diagnosis of schizophrenia. Regardless of whether oxidative stress can be attributed solely to a diagnosis of schizophrenia or whether it is due to other factors associated with schizophrenia, the available evidence is in support of increased oxidative stress-induced cellular damage of macromolecules which may play a role in the phenomenon of accelerated aging presumed to be associated with schizophrenia.

摘要

有几条证据表明,精神分裂症是一种严重的精神疾病,其特征是妄想、幻觉和思维障碍,与加速衰老有关。衰老的自由基(氧化应激)理论假设,衰老的发生是由于氧相关反应产生的自由基对细胞成分和结缔组织造成的损伤。精神分裂症与氧化应激和慢性炎症有关,这两者似乎也以正反馈的方式相互促进。由于氧化应激增加和蛋白质修复和维持系统失效,导致受损大分子的积累,这是细胞和机体水平衰老的一个指标。与年龄匹配的健康对照组相比,精神分裂症患者的氧化细胞损伤标志物水平更高,如蛋白质羰基、脂质过氧化产物和 DNA 羟化产物。潜在的混杂因素,如抗精神病药物、吸烟、社会经济地位和不健康的生活方式,使得不可能仅仅将与衰老相关的变化或氧化应激的更早发生归因于精神分裂症的诊断。无论氧化应激是否可以仅仅归因于精神分裂症的诊断,或者是否是由于与精神分裂症相关的其他因素引起的,现有的证据都支持增加氧化应激诱导的大分子细胞损伤,这可能在与精神分裂症相关的加速衰老现象中起作用。

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