Maes Michael, Mihaylova Ivanka, Kubera Marta, Uytterhoeven Marc, Vrydags Nicolas, Bosmans Eugene
Maes Clinics, Wilrijk - Antwerp, Belgium.
Neuro Endocrinol Lett. 2009;30(6):715-22.
There is now evidence that major depression and myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are accompanied by partially overlapping pathophysiological mechanisms, i.e. activation of various inflammatory and oxidative & nitrosative (IO&NS) pathways.
The aim of the present study was to examine the urinary excretion of 8-hydroxy-deoxyguanosine (8-OhdG), a marker of oxidative damage to DNA, in depression; ME/CFS; and depression and ME/CFS.
Toward this end, morning urine was sampled for the assays of 8-OHdG and creatinine, in 44 patients with ME/CFS; 25 with major depression; 23 with depression and ME/CFS; and 17 normal controls. Severity of fatigue and somatic symptoms was measured by means of the Fibromyalgia and CFS Rating (FF) scale.
We found that 49.0% of the variance in the urinary excretion of 8-OHdG was predicted by the regression on creatinine. Consequently, the urinary 8-OHdG excretion should be expressed as the residualized 8-OHdG values after partialling out the effects of creatinine and not by computing the 8-OHdG / creatinine ratio. We found that the residualized urinary excretion of 8-OHdG (adjusted for creatinine) was significantly higher in patients with depression and ME/CFS than in normal controls and all other patients. In the patient group, there were significant correlations between the urinary 8-OHdG and the total score on the FF scale and sadness and flu-like malaise.
The findings show increased oxidatively generated DNA damage in patients with major depression and ME/CFS and, therefore, further extent the role played by IO&NS pathways in the pathophysiology of both disorders. Since oxidatively damage to DNA is a risk factor for atherosclerosis and neurodegeneration, our results also explain previous findings on increased cardiovascular morbidity in depression and ME/CFS, and neurodegenerative processes in depression.
目前有证据表明，重度抑郁症和肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）伴有部分重叠的病理生理机制，即各种炎症以及氧化与亚硝化（IO&NS）途径的激活。
本研究旨在检测抑郁症、ME/CFS以及抑郁症合并ME/CFS患者中8-羟基脱氧鸟苷（8-OhdG）的尿排泄情况，8-OhdG是DNA氧化损伤的标志物。
为此，对44例ME/CFS患者、25例重度抑郁症患者、23例抑郁症合并ME/CFS患者以及17名正常对照者采集晨尿，用于检测8-OHdG和肌酐。通过纤维肌痛和慢性疲劳综合征评定（FF）量表测量疲劳和躯体症状的严重程度。
我们发现，8-OHdG尿排泄量49.0%的变异可通过肌酐回归预测。因此，尿8-OHdG排泄量应以排除肌酐影响后的残差8-OHdG值表示，而非通过计算8-OHdG/肌酐比值。我们发现，抑郁症合并ME/CFS患者经肌酐校正后的8-OHdG残差尿排泄量显著高于正常对照者及所有其他患者组。在患者组中，尿8-OHdG与FF量表总分、悲伤情绪以及流感样不适之间存在显著相关性。
研究结果显示，重度抑郁症和ME/CFS患者氧化所致的DNA损伤增加，因此进一步扩展了IO&NS途径在这两种疾病病理生理学中的作用。由于DNA氧化损伤是动脉粥样硬化和神经退行性变的危险因素，我们的结果也解释了先前关于抑郁症和ME/CFS中心血管发病率增加以及抑郁症中神经退行性变过程的研究发现。
