Department of Genetics, University Hospital, PTB, 21070 Dijon, France.
Psychiatry Res. 2011 Apr 30;186(2-3):244-7. doi: 10.1016/j.psychres.2010.07.030.
To test the hypothesis that the oxidative stress consistently detected in the peripheral blood of patients with depressive disorder impacts on the functionally relevant brain region, the expression level of nine major genes of the stress response and repair systems has been quantified in the prefrontal cortex of 24 depressive and 12 control subjects. These genes were: superoxide dismutase (SOD1), SOD2, catalase (CAT), gluthatione peroxidase 1 (GPx1), 8-oxoguanine DNA glycosylase (OGG1), nei-like 1 (NEIL1), methionine sulphoxide reductase A (MSRA), telomere repeat-binding factor 2 (TERF2) and C-FOS. Telomere length (a maker of chronic exposure to oxidative stress) has been measured in the DNA of the occipital cortex. No significant difference has been found between the compared groups. It must be concluded that the pathogenic role of the oxidative stress in the cerebral mechanism of depression cannot be inferred from the alteration of peripheral parameters.
为了验证外周血中抑郁障碍患者持续存在的氧化应激是否影响到功能相关的脑区这一假说,研究人员对 24 名抑郁患者和 12 名对照组受试者的前额叶皮层中的 9 种主要应激反应和修复系统的基因表达水平进行了定量分析。这些基因包括:超氧化物歧化酶 1(SOD1)、超氧化物歧化酶 2(SOD2)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶 1(GPx1)、8-氧鸟嘌呤 DNA 糖基化酶(OGG1)、neil 样 1(NEIL1)、蛋氨酸亚砜还原酶 A(MSRA)、端粒重复结合因子 2(TERF2)和 C-FOS。还测量了枕叶皮层 DNA 中的端粒长度(氧化应激慢性暴露的标志物)。比较组之间未发现显著差异。因此可以得出结论,外周参数的改变不能推断氧化应激在抑郁的大脑机制中的致病作用。