Increase of uric acid and purine compounds in biological fluids of multiple sclerosis patients

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• 作者：Angela M. Amorini ; Axel Petzold ; Barbara Tavazzi ; Judith Eikelenboom ; Geoffrey Keir ; Antonio Belli ; Gavin Giovannoni ; Valentina Di Pietro ; Chris Polman ; Serafina D'Urso ; Roberto Vagnozzi ; Bernard Uitd
• 关键词：Multiple sclerosis ; Uric acid ; Purine compounds ; Cerebrospinal fluid ; Serum ; HPLC ; Energy metabolism ; Oxidative stress ; Nitrosative stress
• 刊名：Clinical Biochemistry
• 出版年：2009
• 出版时间：July 2009
• 年：2009
• 卷：42
• 期：10-11
• 页码：1001-1006
• 全文大小：247 K

文摘

Objectives

In this study, the concentrations of uric acid, purine profile and creatinine in samples of cerebrospinal fluid and serum of multiple sclerosis (MS) patients were measured by HPLC and compared with corresponding values recorded in patients without MS (cerebrospinal fluid) and healthy subjects (serum).

Design and methods

All samples were deproteinized with ultrafiltration (which ensures minimal sample manipulation and efficient protein removal) and then assayed for the synchronous HPLC separation of uric acid, hypoxanthine, xanthine, inosine, adenosine, guanosine and creatinine.

Results

The values of all compounds assayed were significantly higher in both biological fluids of MS patients with respect to values measured in controls. In particular, serum hypoxanthine, xanthine, uric acid and sum of oxypurines were, respectively, 3.17, 3.11, 1.23 and 1.27-fold higher in these patients than corresponding values recorded in controls (p < 0.001).

Conclusions

Differently from what previously reported, we here demonstrate that all purine compounds, including uric acid, are elevated in biological fluids of MS patients. Reinforced by the trend observed for creatinine, this corroborates the notion of sustained purine catabolism, possibly due to imbalance in ATP homeostasis, under these pathological conditions. These results cast doubt on the hypothesis that uric acid is depleted in MS because of increased oxidative stress, rather suggesting that this disease causes a generalized increase in purine catabolism. As observed in other pathological states, uric acid, purine compounds and creatinine, can be considered markers of metabolic energy imbalance rather than of reactive oxygen species, even in MS.