No evidence of exogenous origin for the abnormal glutathione redox state in schizophrenia.
No evidence of exogenous origin for the abnormal glutathione redox state in schizophrenia.
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DOI：
10.1016/j.schres.2013.02.001
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发表时间：
2013-05
影响因子：
4.5
通讯作者：
Hong LE
中科院分区：
文献类型：
--
作者：
Ballesteros A;Jiang P;Summerfelt A;Du X;Chiappelli J;O'Donnell P;Kochunov P;Hong LE
精神分裂症与低谷胱甘肽（GSH）有关，谷胱甘肽是天然防御氧化应激的最重要底物之一。这种异常通常归因于遗传或其他病理原因。然而，精神分裂症患者的低GSH也可能是由于抗氧化剂消耗不足或其他外源性因素造成的。我们评估了GSH与精神分裂症患者的饮食、吸烟和药物治疗状况的关系。我们招募了54名参与者（29名精神分裂症患者和25名正常对照）。抗氧化剂饮食来源问题用于估计参与者饮食中的总抗氧化能力（TAC）。测定GSH和氧化型谷胱甘肽（GSSG）。我们发现，与对照组相比，患者的GSH显著降低（p < 0.001），而%GSSG高2至5倍（p = 0.023）。与对照组相比，精神分裂症患者中没有发现TAC饮食摄入量较低的证据;在患者饮食中发现名义上较高的TAC水平（p=0.02）。对个别食物类别的消费分析也没有发现精神分裂症患者饮食中抗氧化剂摄入减少的证据。吸烟和药物治疗也不能显著预测GSH缺乏。然而，有一个显着的吸烟诊断相互作用的GSH（p=0.026），吸烟与较高的GSH水平在对照组，而吸烟的患者与这种影响无关。精神分裂症患者可能有一个受损的谷胱甘肽合成上调，通常发生由于吸烟诱导的抗氧化反应。与对照组相比，服用氯氮平的患者（p = 0.005）和服用其他抗精神病药物的患者（p < 0.001）单独存在较低的GSH。总之，没有一个外源性来源在解释患者谷胱甘肽途径异常中发挥了重要作用。因此，谷胱甘肽氧化还原异常的状态可能是精神分裂症病理生理学的一部分。
Schizophrenia has been associated with low glutathione (GSH), one of the most important substrates for natural defense against oxidative stress. This abnormality is often attributed to genetic or other pathological causes. However, low GSH in schizophrenia could also be due to insufficient antioxidant consumption or other exogenous factors. We evaluated GSH in relation to diet, smoking, and medication status in schizophrenia patients. We recruited 54 participants (29 schizophrenia patients and 25 normal controls). The Antioxidant Dietary Source Questions was used to estimate the total antioxidant capacity (TAC) from participants’ diet. GSH and the oxidized form of glutathione (GSSG) were assayed. We found that GSH was significantly lower (p < 0.001) while %GSSG was 2 to 5 fold higher (p = 0.023) in patients compared with controls. No evidence for lower TAC dietary intake was found in schizophrenia patients compared with controls; rather nominally higher TAC level was found in the patients diet (p=0.02). Analysis of consumption of individual food categories also failed to find evidence of reduced dietary antioxidant intake in schizophrenia patients. Smoking and medications did not significantly predict the GSH deficit either. However, there was a significant smoking by diagnosis interaction on GSH (p=0.026) such that smoking was associated with higher GSH level in controls while smoking in patients was not associated with this effect. Schizophrenia patients may have an impaired upregulation of GSH synthesis that normally occurs due to smoking-induced antioxidative response. Lower GSH was independently present in patients on clozapine (p = 0.005) and patients on other antipsychotics (p < 0.001) compared with controls. In conclusion, none of the exogenous sources played a major role in explaining abnormalities in the glutathione pathway in patients. The state of abnormal glutathione redox may therefore be a part of schizophrenia pathophysiology.
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影响因子：
6.1
作者：
Huber, WW;Prustomersky, S;Schulte-Hermann, R
通讯作者：
Schulte-Hermann, R
影响因子：
6.6
作者：
Harvey, Philip D.;Velligan, Dawn I.;Bellack, Alan S.
通讯作者：
Bellack, Alan S.
影响因子：
3.6
作者：
Kuloglu, M;Ustundag, B;Cinkilinc, N
通讯作者：
Cinkilinc, N
影响因子：
2.9
作者：
GRIFFITH, OW
通讯作者：
GRIFFITH, OW
影响因子：
3.2
作者：
Dakhale, G;Khanzode, S;Turankar, A
通讯作者：
Turankar, A