Dalgiç Buket, Sönmez Nesrin, Biberoğlu Gürsel, Hasanoğlu Alev, Erbaş Deniz
Department of Pediatric Gastroenterology, Gazi University Faculty of Medicine, Cayyolu, Ankara, Turkey.
Turk J Gastroenterol. 2005 Mar;16(1):7-11.
BACKGROUND/AIMS: Oxygen free radicals have an important role in the pathogenesis of acute and chronic liver disease. Free radical formation and oxidative damage, probably mediated with copper accumulation, are important in Wilson's disease pathogenesis. This study was performed to determine if accumulating copper in Wilson's disease is a cause of further oxidant stress compared to non-Wilsonian liver disease.
In this study, we investigated plasma malondialdehyde and nitric oxide levels to estimate the oxidant stress and total antioxidant capacity and vitamin E/cholesterol, vitamin C and beta-carotene levels to estimate the antioxidant status of patients. The groups investigated included 24 patients with Wilson's disease (group I), 25 patients with non-Wilsonian chronic liver disease (group II) and 23 healthy controls (group III). Wilson's disease and non-Wilson's disease patients were divided into subgroups according to disease stage (i.e. chronic hepatitis and cirrhosis) and all parameters were compared between subgroups and controls.
Malondialdehyde and nitric oxide levels were higher than controls in groups I and II (p=0.013, p=0.01), but these levels did not differ between the Wilson's disease and non-Wilson's disease groups. The parameters were also evaluated with respect to the disease stage (i.e. chronic hepatitis and cirrhosis), and there was no difference between groups I and II. Although malondialdehyde and nitric oxide levels were significantly different between both disease stage groups and the controls, we observed decreased vitamin C and beta-carotene levels only in cirrhosis stage (p=0.01, p=0.01).
We observed the presence of oxidant stress unrelated to the etiology of the liver disorder in our study. Deficiency of the major antioxidants, vitamin C and beta-carotene, develops as the disease stage advances from chronic hepatitis to cirrhosis.
背景/目的:氧自由基在急慢性肝病的发病机制中起重要作用。自由基的形成和氧化损伤(可能由铜蓄积介导)在威尔逊病的发病机制中很重要。本研究旨在确定与非威尔逊病性肝病相比,威尔逊病中蓄积的铜是否会导致进一步的氧化应激。
在本研究中,我们检测了血浆丙二醛和一氧化氮水平以评估氧化应激,检测了总抗氧化能力、维生素E/胆固醇、维生素C和β-胡萝卜素水平以评估患者的抗氧化状态。研究组包括24例威尔逊病患者(I组)、25例非威尔逊病性慢性肝病患者(II组)和23名健康对照者(III组)。威尔逊病和非威尔逊病患者根据疾病阶段(即慢性肝炎和肝硬化)分为亚组,并对亚组与对照组之间的所有参数进行比较。
I组和II组的丙二醛和一氧化氮水平高于对照组(p = 0.013,p = 0.01),但威尔逊病组和非威尔逊病组之间这些水平无差异。还根据疾病阶段(即慢性肝炎和肝硬化)对参数进行了评估,I组和II组之间无差异。虽然两个疾病阶段组与对照组之间的丙二醛和一氧化氮水平有显著差异,但我们仅在肝硬化阶段观察到维生素C和β-胡萝卜素水平降低(p = 0.01,p = 0.01)。
在我们的研究中,我们观察到存在与肝脏疾病病因无关的氧化应激。随着疾病阶段从慢性肝炎进展到肝硬化,主要抗氧化剂维生素C和β-胡萝卜素缺乏会逐渐出现。