Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis
Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis
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DOI：
10.1177/0269881119845820
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发表时间：
2019-04
影响因子：
4.1
通讯作者：
Sakiko Tsugawa;Y. Noda;R. Tarumi;Y. Mimura;Kazunari Yoshida;Y. Iwata;Muhammad Elsalhy;Minori Kuromiya;S. Kurose;F. Masuda;S. Morita;K. Ogyu;E. Plitman;M. Wada;T. Miyazaki;A. Graff-Guerrero;M. Mimura;S. Nakajima
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文献类型：
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作者：
Sakiko Tsugawa;Y. Noda;R. Tarumi;Y. Mimura;Kazunari Yoshida;Y. Iwata;Muhammad Elsalhy;Minori Kuromiya;S. Kurose;F. Masuda;S. Morita;K. Ogyu;E. Plitman;M. Wada;T. Miyazaki;A. Graff-Guerrero;M. Mimura;S. Nakajima
背景：谷胱甘肽是预防氧化应激的重要抗氧化剂之一。然而，由于对精神分裂症患者谷胱甘肽水平和/或谷胱甘肽相关酶活性的研究结果不一致，谷胱甘肽系统异常与精神分裂症病理生理之间的关系仍不确定。方法：应用Embase、Medline、SqucINFO、PubMed等数据库进行系统的文献检索。对精神分裂症患者和健康对照组的3种代谢物(谷胱甘肽、谷胱甘肽二硫)和总谷胱甘肽(谷胱甘肽+谷胱甘肽二硫化物)水平和5种酶活性(谷胱甘肽过氧化物酶、谷胱甘肽还原酶、谷氨酸半胱氨酸连接酶、谷胱甘肽合成酶和谷胱甘肽S转移酶)进行了检测。用随机效应模型计算标准化均数差值以确定谷胱甘肽水平的组间差异。结果：我们确定了41、9、15、38项研究，以及7项分别检测谷胱甘肽、谷胱甘肽二硫化物、总谷胱甘肽、谷胱甘肽过氧化物酶和谷胱甘肽还原酶的研究。精神分裂症患者的谷胱甘肽和总谷胱甘肽水平均低于对照组，谷胱甘肽过氧化物酶活性低于对照组。未服药的精神分裂症患者的谷胱甘肽水平低于对照组，而首发精神病患者和对照组之间的谷胱甘肽水平没有差异。结论：精神分裂症患者的谷胱甘肽氧化还原循环可能存在谷胱甘肽缺陷和异常。然而，由于研究了整个谷胱甘肽系统的研究很少，还需要进一步的研究来更好地了解精神分裂症中谷胱甘肽功能受损的原因，这可能为开发这种疾病的新治疗策略铺平道路。
Background: Glutathione is among the important antioxidants to prevent oxidative stress. However, the relationships between abnormality in the glutathione system and pathophysiology of schizophrenia remain uncertain due to inconsistent findings on glutathione levels and/or glutathione-related enzyme activities in patients with schizophrenia. Methods: A systematic literature search was conducted using Embase, Medline, PsycINFO, and PubMed. Original studies, in which three metabolite levels (glutathione, glutathione disulfide, and total glutathione (glutathione+glutathione disulfide)) and five enzyme activities (glutathione peroxidase, glutathione reductase, glutamate-cysteine ligase, glutathione synthetase, and glutathione S-transferase) were measured with any techniques in both patients with schizophrenia and healthy controls, were included. Standardized mean differences were calculated to determine the group differences in the glutathione levels with a random-effects model. Results: We identified 41, 9, 15, 38, and seven studies which examined glutathione, glutathione disulfide, total glutathione, glutathione peroxidase, and glutathione reductase, respectively. Patients with schizophrenia had lower levels of both glutathione and total glutathione and decreased activity of glutathione peroxidase compared to controls. Glutathione levels were lower in unmedicated patients with schizophrenia than those in controls while glutathione levels did not differ between patients with first-episode psychosis and controls. Conclusions: Our findings suggested that there may be glutathione deficits and abnormalities in the glutathione redox cycle in patients with schizophrenia. However, given the small number of studies examined the entire glutathione system, further studies are needed to elucidate a better understanding of disrupted glutathione function in schizophrenia, which may pave the way for the development of novel therapeutic strategies in this disorder.