Successful interferon therapy reverses enhanced hepatic iron accumulation and lipid peroxidation in chronic hepatitis C

Kageyama, Fujito; Kobayashi, Yoshimasa; Kawasaki, Tsunehisa; Toyokuni, Shinya; Uchida, Kôji; Nakamura, Hirotoshi

doi:10.1111/j.1572-0241.2000.01979.x

Cited by 87 publications

(58 citation statements)

References 33 publications

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“…Infection with HCV is associated with increased levels of ROS/RNS and decreased antioxidant levels in patients [71][72][73][74]. Patients infected with HCV show increases in lipid peroxidation levels in liver samples, serum, and peripheral blood mononuclear cells [72,[75][76][77][78][79][80].…”

Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

“…Patients infected with HCV show increases in lipid peroxidation levels in liver samples, serum, and peripheral blood mononuclear cells [72,[75][76][77][78][79][80]. In addition, other indicators of oxidative stress such as 4-hydroxynonenal and 8-hydroxydeoxyguanosine were found to be increased in HCV [72,74,[80][81][82][83]. The content of GSH decreased in the blood, liver, and lymphatic system, whereas that of GSSG increased, indicating a high glutathione turnover [83].…”

Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

“…The mechanisms for more severe increases of oxidative and nitrosative stresses during HCV disease may include chronic inflammation (i.e., phagocytic NAD(P)H oxidase activation) and overload of iron, which is more specific to HCV [72,75,84]. Furthermore, the production of ROS in the hepatocytes may lead to the activation of KC [85].…”

Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

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Role of free radicals in liver diseases

2009

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Reactive oxygen and nitrogen species (ROS and RNS) are produced by metabolism of normal cells. However, in liver diseases, redox is increased thereby damaging the hepatic tissue; the capability of ethanol to increase both ROS/RNS and peroxidation of lipids, DNA, and proteins was demonstrated in a variety of systems, cells, and species, including humans. ROS/RNS can activate hepatic stellate cells, which are characterized by the enhanced production of extracellular matrix and accelerated proliferation. Cross-talk between parenchymal and nonparenchymal cells is one of the most important events in liver injury and fibrogenesis; ROS play an important role in fibrogenesis throughout increasing platelet-derived growth factor. Most hepatocellular carcinomas occur in cirrhotic livers, and the common mechanism for hepatocarcinogenesis is chronic inflammation associated with severe oxidative stress; other risk factors are dietary aflatoxin B 1 consumption, cigarette smoking, and heavy drinking. Ischemia-reperfusion injury affects directly on hepatocyte viability, particularly during transplantation and hepatic surgery; ischemia activates Kupffer cells which are the main source of ROS during the reperfusion period. The toxic action mechanism of paracetamol is focused on metabolic activation of the drug, depletion of glutathione, and covalent binding of the reactive metabolite N-acetyl-pbenzoquinone imine to cellular proteins as the main cause of hepatic cell death; intracellular steps critical for cell death include mitochondrial dysfunction and, importantly, the formation of ROS and peroxynitrite. Infection with hepatitis C is associated with increased levels of ROS/RNS and decreased antioxidant levels. As a consequence, antioxidants have been proposed as an adjunct therapy for various liver diseases.

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Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

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Role of free radicals in liver diseases

2009

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“…The mechanisms underlying HCV-associated liver injury are imperfectly understood. Several lines of evidence indicate that increased oxidative stress is an important pathogenetic mechanism in CHC (3)(4)(5)(6)(7)(8)(9). HCV core and nonstructural proteins have been shown to cause transcriptional modulation as either trans-activators or trans-suppressors of cellular signaling pathways through interference with intracellular oxidation/reduction reactions (10)(11)(12).…”

mentioning

confidence: 99%

Reciprocal Effects of Micro-RNA-122 on Expression of Heme Oxygenase-1 and Hepatitis C Virus Genes in Human Hepatocytes

et al. 2007

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“…Recent studies have documented an association between HCV infection and the presence of both liver and serum markers of oxidative stress. [9][10][11][12][13][14] Furthermore, the expression of HCV core protein in transgenic mice or in hepatoma cells lines alters the liver antioxidant status and promotes lipid peroxidation. 15,16 Ethanol is also known to stimulate the production of reactive oxygen species and hydroxyethyl free radicals and to lower hepatic antioxidant defense.…”

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confidence: 99%

Moderate alcohol consumption increases oxidative stress in patients with chronic hepatitis C

et al. 2003

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The mechanisms by which alcohol consumption worsens the evolution of chronic hepatitis C (CHC) are poorly understood. We have investigated the possible interaction between hepatitis C virus (HCV) and ethanol in promoting oxidative stress. Circulating IgG against human serum albumin (HSA) adducted with malondialdehyde (MDA-HSA), 4-hydroxynonenal (HNE-HSA), or arachidonic acid hydroperoxide (AAHP-HSA) and against oxidized cardiolipin (Ox-CL) were evaluated as markers of oxidative stress in 145 CHC patients with different alcohol consumption, 20 HCV-free heavy drinkers (HD) without liver disease, and 50 healthy controls. Anti-MDA IgG was increased in CHC patients irrespective of alcohol intake as well as in the HD group. CHC patients with moderate alcohol intake (<50 g ethanol/d), but not HD, also had significantly higher values of anti-AAHP-HSA, anti-HNE-HSA, and anti-Ox-CL IgG (P < .05) than controls. A further elevation (P < .001) of these antibodies was evident in CHC patients with heavy alcohol intake (>50 g ethanol/d). Anti-AAHP and anti-Ox-CL IgG above the 95th percentile in the controls were observed in 24% to 26% of moderate and 58% to 63% of heavy drinkers but only in 6% to 9% of the abstainers. The risk of developing oxidative stress during CHC was increased 3-fold by moderate and 13-to 24-fold by heavy alcohol consumption. Heavy drinking CHC patients had significantly more piecemeal necrosis and fibrosis than abstainers. Diffuse piecemeal necrosis was 4-fold more frequent among alcohol-consuming patients with lipid peroxidation-related antibodies than among those without these antibodies. In conclusion, even moderate alcohol consumption promotes oxidative stress in CHC patients, suggesting a role for oxidative injury in the worsening of CHC evolution by alcohol. (HEPATOLOGY 2003; 38:42-49.)

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Successful interferon therapy reverses enhanced hepatic iron accumulation and lipid peroxidation in chronic hepatitis C

Cited by 87 publications

References 33 publications

Role of free radicals in liver diseases

Role of free radicals in liver diseases

Reciprocal Effects of Micro-RNA-122 on Expression of Heme Oxygenase-1 and Hepatitis C Virus Genes in Human Hepatocytes

Moderate alcohol consumption increases oxidative stress in patients with chronic hepatitis C

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