Biancini Giovana B, Vanzin Camila S, Rodrigues Daiane B, Deon Marion, Ribas Graziela S, Barschak Alethéa G, Manfredini Vanusa, Netto Cristina B O, Jardim Laura B, Giugliani Roberto, Vargas Carmen R
Programa de Pós-Graduação em Ciências Biológicas:Bioquímica, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
Biochim Biophys Acta. 2012 Feb;1822(2):226-32. doi: 10.1016/j.bbadis.2011.11.001. Epub 2011 Nov 6.
Fabry disease is an X-linked inborn error of glycosphingolipid catabolism due to deficient activity of α-galactosidase A that leads to accumulation of the enzyme substrates, mainly globotriaosylceramide (Gb3), in body fluids and lysosomes of many cell types. Some pathophysiology hypotheses are intimately linked to reactive species production and inflammation, but until this moment there is no in vivo study about it. Hence, the aim of this study was to investigate oxidative stress parameters, pro-inflammatory cytokines and Gb3 levels in Fabry patients under treatment with enzyme replacement therapy (ERT) and finally to establish a possible relation between them. We analyzed urine and blood samples of patients under ERT (n=14) and healthy age-matched controls (n=14). Patients presented decreased levels of antioxidant defenses, assessed by reduced glutathione (GSH), glutathione peroxidase (GPx) activity and increased superoxide dismutase/catalase (SOD/CAT) ratio in erythrocytes. Concerning to the damage to biomolecules (lipids and proteins), we found that plasma levels of malondialdehyde (MDA) and protein carbonyl groups and di-tyrosine (di-Tyr) in urine were increased in patients. The pro-inflammatory cytokines IL-6 and TNF-α were also increased in patients. Urinary Gb3 levels were positively correlated with the plasma levels of IL-6, carbonyl groups and MDA. IL-6 levels were directly correlated with di-Tyr and inversely correlated with GPx activity. This data suggest that pro-inflammatory and pro-oxidant states occur, are correlated and seem to be induced by Gb3 in Fabry patients.
法布里病是一种X连锁的糖鞘脂分解代谢先天性缺陷疾病,由于α-半乳糖苷酶A活性不足,导致酶底物主要是球三糖神经酰胺(Gb3)在多种细胞类型的体液和溶酶体中蓄积。一些病理生理学假说是与活性物质产生和炎症密切相关的,但直到目前尚无关于此的体内研究。因此,本研究的目的是调查接受酶替代疗法(ERT)治疗的法布里病患者的氧化应激参数、促炎细胞因子和Gb3水平,并最终确定它们之间的可能关系。我们分析了接受ERT治疗的患者(n = 14)和年龄匹配的健康对照者(n = 14)的尿液和血液样本。患者红细胞中通过还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GPx)活性评估的抗氧化防御水平降低,超氧化物歧化酶/过氧化氢酶(SOD/CAT)比值升高。关于生物分子(脂质和蛋白质)的损伤,我们发现患者血浆丙二醛(MDA)水平、蛋白羰基以及尿液中的二酪氨酸(di-Tyr)升高。患者的促炎细胞因子IL-6和TNF-α也升高。尿Gb3水平与IL-6、羰基和MDA的血浆水平呈正相关。IL-6水平与di-Tyr直接相关,与GPx活性呈负相关。这些数据表明,法布里病患者存在促炎和促氧化状态,它们相互关联,似乎由Gb3诱导。