Exley Christopher, Mamutse Godwin, Korchazhkina Olga, Pye Eleanor, Strekopytov Stanislav, Polwart Anthony, Hawkins Clive
Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK.
Mult Scler. 2006 Oct;12(5):533-40. doi: 10.1177/1352458506071323.
Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing-remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.
多发性硬化症（MS）是一种慢性、免疫介导的中枢神经系统脱髓鞘疾病，病因尚不明确。一种共识观点认为，该疾病是环境因素与易感基因相互作用的结果。我们运用了一系列分析技术来确定：i）氧化损伤标志物；ii）铁；iii）环境毒素铝及其拮抗剂硅在复发缓解型多发性硬化症（RRMS）和继发进展型多发性硬化症（SPMS）中的尿排泄量是否发生改变。未发现尿中氧化生物标志物丙二醛（MDA）和硫代巴比妥酸反应物（TBARS）的浓度是MS炎症性疾病的有用指标。然而，另一种炎症和氧化应激潜在标志物铁的尿浓度在SPMS中显著升高（P<0.01），在RRMS中虽有升高但不显著（P>0.05）。RRMS（P<0.001）和SPMS（P<0.05）中尿铝浓度也显著升高，以至于前者的铝排泄水平与接受金属螯合治疗的个体所观察到的水平相似。MS患者尿中硅的排泄量较低，在SPMS中尤为显著（P<0.05）。尿中铁排泄增加支持了铁代谢异常在MS中的作用。尿铝排泄水平与铝中毒时所见相似，这表明铝可能是与MS病因相关的一个迄今未被认识的环境因素。如果铝与MS有关，那么增加其天然拮抗剂硅的饮食摄入量可能是一种治疗选择。
