title: [Iron and liver disease].
abstract: Free iron in the liver is believed to facilitate the formation of reactive oxygen species (ROS), including hydroxyl radicals (*OH), which cause oxidative damage of numerous cellular components such as lipids, proteins, and nucleic acids, and also upregulate collagen synthesis. The *OH radical is known to generate promutagenic bases such as 8-hydroxy-2-deoxyguanosine (8-OHdG). In cases with chronic hepatitis C, long-term iron reduction therapy reduced the activity of hepatitis, suppressed fibrosis, and prevented hepatocarcinogenesis. In nonalcoholic steatohepatitis (NASH) livers, hepatic iron accumulation as well as oxidative DNA damage significantly increased. Humoral factor(s) in NASH serum may upregulate DMT1 expression in small intestine. Iron reduction therapy for NASH patients has a potential to reduce disease activity as well as hepatic oxidative damage.
authors.forename: Koji
authors.initials: K
authors.lastname: Miyanishi
authors.forename: Junji
authors.initials: J
authors.lastname: Kato
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000378:metabolism*; D006801:Humans; D007501:Iron / Q000378:metabolism*; D007583:Jejunum / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease / Q000235:genetics / Q000378:metabolism*; D018384:Oxidative Stress
chemical_list: D000080242:8-Hydroxy-2'-Deoxyguanosine; D007501:Iron; D003849:Deoxyguanosine