Increased lipid peroxidation in patients with non‐alcoholic fatty liver disease and chronic hepatitis C as measured by the plasma level of 8‐isoprostane

Konishi, Masayoshi; Iwasa, Motoh; Araki, Jun; Kobayashi, Yoshinao; Katsuki, Akira; Sumida, Yasuhiro; Nakagawa, Naoki; Kojima, Yuji; Watanabe, Shozo; Adachi, Yukihiko; Kaito, Masahiko

doi:10.1111/j.1440-1746.2006.04420.x

Cited by 79 publications

(63 citation statements)

References 35 publications

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“…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].…”

Section: Viral Hepatitis and Free Radicalsmentioning

confidence: 99%

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%

Role of free radicals in liver diseases

2009

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“…Changes in the lipid body compositions have been reported for patients with insulin-resistant NAFLD and have been characterized by 1) reduction in long-chain fatty acids, 2) increased n-6/n-3 PUFA ratios in liver and adipose tissue, 3) increased 18:1 n-9 trans levels in adipose tissue, 4) and elevated markers of hepatic lipid peroxidation and protein oxidation Konishi et al, 2006).…”

Section: Polyunsaturated Fatty Acids In Nonalcoholic Hepatic Steatosimentioning

confidence: 99%

Molecular Mechanisms and Therapeutic Targets in Steatosis and Steatohepatitis

Anderson

Borlak²

2008

Pharmacol Rev

342

255

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“…While it might be expected that enhanced lipid peroxidation in NAFLD would be dependent, at least partially, on some lipidamic measures, there was little published support for such a correlation to date. Konishi et al [30] found no significant associations of plasma iPF 2α -Ⅲ with TC and TG in patients with NAFLD. In addition, Madan et al [31] failed to find relationship between oxidant stress and ALT levels in either NAFLD patients or diseased controls.…”

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confidence: 99%