IMBALANCE OF OXIDANTS AND ANTIOXIDANT SYSTEMS IN SUBJECTS WITH CIRRHOSIS (original) (raw)
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Medical Hypotheses, 2011
Patients with liver cirrhosis are prone to serious complications by almost all systems, leading to high morbidity rates and even death. Although the functional and structural derangement of diverse vital organs developed in the course of advanced liver disease is the result of one entity (cirrhosis) there are various treatment modalities for each system's complications, which are often ineffective. Identification of the link which connects the complications of cirrhosis from diverse systems might lead to a global, simple and more effective treatment approach for patients with cirrhosis. Accumulating evidence from experimental and clinical studies suggests that intestinal barrier dysfunction and subsequent gut-derived endotoxemia represent an important common pathogenetic mechanism in the development of diverse complications of cirrhosis. Intestinal oxidative stress seems to be a pivotal factor of gut barrier dysfunction in cirrhosis through promotion of enterocyte apoptosis, modulation of intestinal tight junctions and impairment of intestinal brush border function. In parallel, oxidative stress plays a fundamental role in the aggravation of liver injury and in the structural and/or functional derangements of diverse organs complicating the course of cirrhosis. Our hypothesis is that antioxidant treatments could prevent in a global way virtually all cirrhosis-related complications acting in two crucial levels in the pathophysiological cascade of events: (a) in a primary level, which is the gut-liver axis by ameliorating gut-derived endotoxemia, through prevention of intestinal oxidative stress and its associated gut barrier dysfunction, concurrently conferring direct antioxidant protection in the liver tissue and (b) in a secondary level, which refers to the diverse organs whose function is affected by liver cirrhosis, by preventing their oxidant-related structural and functional derangements.
In: Antioxidants: New Research Oxidants and Antioxidants in Liver Disease
Production of reactive oxygen and nitrogen species is an integral part of normal human metabolism and has been proved to have both beneficial and deleterious effects in various diseases including liver diseases. Normally neutralization of these oxidizing molecules occurs through their interaction with a complex system of antioxidant processes mediated by endogenous (superoxide dismutases, glutathione, albumin, billirubin etc.) and exogenous (polyphenols, vitamins etc.) molecules. In the last few decades numerous in vitro and in vivo studies have examined the effect of oxidants and antioxidants in the initiation and progression of alcohol-induced liver damage, toxic liver injury, liver ischemia/reperfusion injury, viral hepatitis, autoimmune hepatitis, cirrhosis, primary billiary cirrhosis, primary sclerosing cholangiitis and hepatocellular carcinoma. Non-parenchymal liver cells, like Kupffer cells and hepatic stellate cells, have also been reported to play an important role in the o...
Interrelation of inflammation and oxidative stress in liver cirrhosis
Experimental and Therapeutic Medicine
Recently, the trend of research has been focused on the role of hematological indicators in assessing the activities of various diseases. The aim of the present study was to determine the usefulness of such hematological indicators for assessment of the relationship between inflammation and oxidative stress in order to provide new predictive tools for a non-invasive investigation of disease outcome for liver cirrhosis patients. A total of 35 subjects with compensated or decompensated liver cirrhosis and 10 age-matched healthy volunteers were included in this study. The patients were divided into two groups: Group 1, patients with toxic metabolic cirrhosis due to ethanol consumption; group 2, patients with liver cirrhosis following hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. Using hematological data obtained after the complete counting of peripheral blood cells, the monocyte/lymphocyte (MLR), neutrophil/lymphocyte (NLR) and platelet/lymphocyte (PLR) ratios as well as systemic immune inflammation biomarkers were determined. The erythrocyte sedimentation ratio (ESR), C-reactive protein (CRP), fibrinogen and biochemical parameters related to liver function were also registered. Thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCARB), and total antioxidant capacity (TAC) were also investigated in the peripheral blood samples of healthy subjects and liver cirrhosis patients. The results revealed that NLR, MLR and PLR were significantly increased in group 2. PLR was significantly increased in group 1 compared with that noted in the control group. TBARS and PCARB were increased in patients from group 1 compared to patients from group 2 and the control group. However, no difference in TAC was found between the liver cirrhosis groups and the control. We showed that the pro-inflammatory status of liver cirrhosis patients can be easily appreciated by NLR, MLR but not PLR. However, the increase in these ratios was not significantly associated with a decrease in the antioxidant capacity and an augmentation of oxidative stress markers for the patients diagnosed with cirrhosis included in the two groups of study.
Oxidative stress has been increasingly implicated in the pathogenesis and progression of liver cirrhosis. Chronic ethanol consumption induces an oxidative stress resulting in increased ferritin levels and thereby iron over load. The study was aimed at evaluating the relation between alcohol consumption and erythrocyte superoxide dismutase (SOD), Glutathione peroxidase (GPx), Malondialdehyde (MDA) activities in liver cirrhosis patients. The study included two groups based on alcohol consumption; subjects taking low alcohol content (Less than 150 g/day.), those consuming high alcohol content (More than 150 g/day), diagnosed as suffering from liver cirrhosis and control group who do not take alcohol and are not suffering from liver cirrhosis. All cirrhotic patients on high alcohol intake in the study group had lower serum SOD (P < 0.0001), GPx (0.0001) and significantly higher MDA levels (P<0.001) than those with subjects taking low alcohol and control group. These results suggest that the decrease in erythrocyte SOD, GPx and increase in MDA levels are related to the alcohol consumption and that may be associated with pathogenesis and progression of liver disease.
Behavior of Oxidative Stress Markers in Alcoholic Liver Cirrhosis Patients
Oxidative Medicine and Cellular Longevity, 2016
Alcohol is the most socially accepted addictive substance worldwide, and its metabolism is related with oxidative stress generation. The aim of this work was to evaluate the role of oxidative stress in alcoholic liver cirrhosis (ALC). This study included 187 patients divided into two groups: ALC, classified according to Child-Pugh score, and a control group. We determined the levels of reduced and oxidized glutathione (GSH and GSSG) and the GSH/GSSG ratio by an enzymatic method in blood. Also, protein carbonyl and malondialdehyde (MDA) content were estimated in serum. MDA levels increased in proportion to the severity of damage, whereas the GSH and GSSG levels decreased and increased, respectively, at different stages of cirrhosis. There were no differences in the GSH/GSSG ratio and carbonylated protein content between groups. We also evaluated whether the active consumption of or abstinence from alcoholic beverages affected the behavior of these oxidative markers and only found dif...
Oxidant stress is a significant feature of primary biliary cirrhosis
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2003
Primary biliary cirrhosis (PBC) is a chronic cholestatic disorder characterised by an immunological, and often granulomatous, attack on bile ducts leading to fibrosis, cirrhosis, liver failure and death. Animal and human studies suggest that oxidant stress plays a key role in progression of other liver diseases, but no comprehensive investigation has been performed previously in PBC. A wide range of lipid peroxidation and antioxidant markers were measured in the blood and urine of 41 patients with histologically confirmed PBC. Lipid peroxidation markers were significantly elevated [plasma and urinary 8-isoprostane, P < 0.001; plasma malondialdehyde (MDA), P = 0.007] compared to age-and sex-matched controls. The most striking antioxidant depletion occurred with plasma total glutathione where levels were significantly reduced (30% of controls). Total serum antioxidant levels were decreased (P = 0.013) and serum selenium and vitamin A were also lower (both P < 0.001); vitamins C and E were normal. Most patients had early disease biochemically and were Child-Pugh grade A. Urinary 8-isoprostane correlated positively with Ludwig stage and markers of hepatic injury and cholestasis. This study clearly demonstrates that oxidant stress, as reflected in a comprehensive spectrum of lipid peroxidation and antioxidant markers, is a significant feature of earlystage PBC. D