Blood cell superoxide dismutase and enolase activities as markers of alcoholic and nonalcoholic liver diseases

Ledig, M.; Doffoël, M; Doffoel, S.; Kopp, P.; Bockel, R; Mandel, P.

doi:10.1016/0741-8329(88)90025-0

Cited by 10 publications

(3 citation statements)

References 30 publications

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“…Ohman and Marklund (1986) found no variation in SOD activity in such patients. Conversely, Ledig et al (1988) observed an increase in SOD in alcoholics with liver disease (steatosis, cirrhosis with or without ascites); this evaluation appeared associated with the degree of liver injury. Such an increase was also reported by Emerit et al (1984) in a restricted population of alcoholics with severe liver injury.…”

Section: Discussionmentioning

confidence: 67%

Oxidative Status in Patients with Alcohol Dependence: A Clinical Study in Taiwan

Peng

Tang

Huang

et al. 2005

Journal of Toxicology and Environmental Health, Part A

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The aim of this study is to examine the relationship between alcohol dependence and oxidative status. The biochemical parameters and antioxidants status were measured among 28 patients with alcohol dependence. Nineteen healthy persons without drinking problem were recruited as the control subjects. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (gamma-GT), and levels of cholesterol, triglyceride (TG), and uric acid were significantly increased in the specimen of patients compared with control. Serum malondialdehyde (MDA) levels of the patients were found to be significantly increased compared with controls and decreased after abstinence. Superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were, respectively, 86% and 37% lower in alcoholic patients. After 14 d of abstinence, SOD activity was significantly reduced by 85%, CAT by 52%, and GPX by 54%, whereas no change was found in activity of glutathione reductase (GR). The duration of alcohol dependence is significantly correlated with the levels of MDA. In addition, the activity of CAT was significantly correlated with MDA levels. The results of this study suggest that oxidative stress occurred during alcohol dependence and subsequently affected the antioxidants mechanisms.

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Section: Discussionmentioning

confidence: 67%

Oxidative Status in Patients with Alcohol Dependence: A Clinical Study in Taiwan

Peng

Tang

Huang

et al. 2005

Journal of Toxicology and Environmental Health, Part A

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“…Data on superoxide dismutase activity, an antioxidant defence enzyme that reduces superoxide to hydrogen peroxide, 21 in the blood of alcoholics are contradictory: increased 8 , 22 , 23 and decreased 23 , 24 activity have been reported. In the present study, differences between the superoxide dismutase activities of alcoholic patients, who continuously consumed excess alcohol, patients with end‐stage non‐alcoholic liver disease and healthy controls were small (Table 2) and probably not important.…”

Section: Discussionmentioning

confidence: 99%

Blood antioxidant levels in patients with alcoholic liver disease correlate with the degree of liver impairment and are not specific to alcoholic liver injury itself

Casteele

Zaman

Zeegers

et al. 2002

Aliment Pharmacol Ther

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Background: Enhanced production of reactive oxygen species may play a pathogenic role in alcoholic liver injury. Aims: To investigate whether various antioxidant parameters in blood are affected in different stages of alcoholic liver disease and how specific the changes are relative to non‐alcoholic cirrhosis. Methods: Patients with alcohol abuse without cirrhosis (n=14), with alcoholic cirrhosis [Child–Pugh scores A (n=9), B (n=5) and C (n=18)] and with non‐alcoholic cirrhosis [Child–Pugh score C (n=6)] and healthy controls (n=13) were studied. Levels of reduced glutathione and glutathione peroxidase activity in blood, erythrocytic superoxide dismutase activity and carotenoids, α‐tocopherol and malondialdehyde in plasma were measured. Results: Levels of reduced glutathione were significantly decreased in Child–Pugh score C cirrhotics, alcoholic or not in origin, whereas oxidized glutathione and glutathione peroxidase activity were not affected. Superoxide dismutase activity and α‐tocopherol levels were not significantly different in the various groups. Carotenoid levels were significantly lower in alcoholic cirrhotics (Child–Pugh score C) vs. controls. Malondialdehyde levels were elevated only in cirrhotics Child–Pugh score C, alcoholic or non‐alcoholic. Conclusions: Levels of reduced glutathione and malondialdehyde reflect the degree of liver impairment, more than the relation with alcohol intake. Decreases in several antioxidant levels are not specific to alcoholic liver injury.

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“…Thus, there is a need for simple non-invasive and definitive markers of early changes in the development of ALD. Several have been proposed including serum beta-hexosaminidase [5,6], increased activity of superoxide dismutase (SOD) and neuron-specific enolase (NSE) in blood cells [7], increased levels of lymphocyte cytochrome P450 CYP2E1 [8]. A metabolomics study in mice revealed two metabolites in urine, N -acetylglutamine and N -acetylglycine, that might be useful markers for ALD [9].…”

Section: Introductionmentioning

confidence: 99%

Identification of serum insulin-like growth factor binding protein 1 as diagnostic biomarker for early-stage alcohol-induced liver disease

Doiron

Patterson

et al. 2013

J Transl Med

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BackgroundAlcohol consumption is a major cause of liver disease in humans. The use and monitoring of biomarkers associated with early, pre-clinical stages of alcohol-induced liver disease (pre-ALD) could facilitate diagnosis and treatment, leading to improved outcomes.MethodsWe investigated the pathological, transcriptomic and protein changes in early stages of pre-ALD in mice fed the Lieber-Decarli liquid diet with or without alcohol for four months to identify biomarkers for the early stage of alcohol induced liver injury. Mice were sampled after 1, 2 and 4 months treatment.ResultsPathological examination revealed a modest increase in fatty liver changes in alcohol-treated mice. Transcriptomics revealed gene alterations at all time points. Most notably, the Igfbp1 (Insulin-Like Growth Factor Binding Protein 1) was selected as the best candidate gene for early detection of liver damage since it showed early and continuously enhanced induction during the treatment course. Consistent with the microarray data, both Igfbp1mRNA expression in the liver tissue and the IGFBP1 serum protein levels showed progressive and significant increases over the course of pre-ALD development.ConclusionsThe results suggest that in conjunction with other tests, serum IGFBPI protein could provide an easily measured biomarker for early detection of alcohol-induced liver injury in humans.

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Blood cell superoxide dismutase and enolase activities as markers of alcoholic and nonalcoholic liver diseases

Cited by 10 publications

References 30 publications

Oxidative Status in Patients with Alcohol Dependence: A Clinical Study in Taiwan

Oxidative Status in Patients with Alcohol Dependence: A Clinical Study in Taiwan

Blood antioxidant levels in patients with alcoholic liver disease correlate with the degree of liver impairment and are not specific to alcoholic liver injury itself

Identification of serum insulin-like growth factor binding protein 1 as diagnostic biomarker for early-stage alcohol-induced liver disease

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