BACKGROUND/AIMS: 8-Hydroxydeoxyguanosine (8-OHdG) is a promutagenic DNA lesion produced by oxygen radicals and is recognized as a useful marker in estimating DNA damage induced by oxidative stress. METHODS: Hepatic expression of 8-OHdG was immunohistochemically investigated in control and diseased human livers. RESULTS: While no positive immunolabeling for 8-OHdG was observed in control livers, 8-OHdG was widely evident in diseased livers. Nuclear expression of 8-OHdG in the hepatocytes and bile duct cells were found in various forms of chronic hepatitis. 8-OHdG-positive hepatocytes were especially abundant in the periportal area with piecemeal necrosis and prominent cell infiltration. The number of positive hepatocytes significantly increased with the progression of severity of chronic hepatitis activity (r(s)=0.68, P<0.05). In alcoholic liver disease, nuclear expression of 8-OHdG was detected in the hepatocytes in the area of alcoholic hepatitis. Regarding primary biliary cirrhosis, 8-OHdG was preferentially detected in the nuclei of injured bile ducts (11 of 12 cases, 91.7%) and occasionally (2 of 12 cases, 16.7%) in the nuclei of hepatocytes around the bile duct lesions. CONCLUSIONS: These results indicate that oxidative DNA damage is common in various forms of chronic liver disease suggesting a possible link between chronic inflammation and hepatocarcinogenesis.
BACKGROUND/AIMS: 8-Hydroxydeoxyguanosine (8-OHdG) is a promutagenic DNA lesion produced by oxygen radicals and is recognized as a useful marker in estimating DNA damage induced by oxidative stress. METHODS: Hepatic expression of 8-OHdG was immunohistochemically investigated in control and diseased human livers. RESULTS: While no positive immunolabeling for 8-OHdG was observed in control livers, 8-OHdG was widely evident in diseased livers. Nuclear expression of 8-OHdG in the hepatocytes and bile duct cells were found in various forms of chronic hepatitis. 8-OHdG-positive hepatocytes were especially abundant in the periportal area with piecemeal necrosis and prominent cell infiltration. The number of positive hepatocytes significantly increased with the progression of severity of chronic hepatitis activity (r(s)=0.68, P<0.05). In alcoholic liver disease, nuclear expression of 8-OHdG was detected in the hepatocytes in the area of alcoholic hepatitis. Regarding primary biliary cirrhosis, 8-OHdG was preferentially detected in the nuclei of injured bile ducts (11 of 12 cases, 91.7%) and occasionally (2 of 12 cases, 16.7%) in the nuclei of hepatocytes around the bile duct lesions. CONCLUSIONS: These results indicate that oxidative DNA damage is common in various forms of chronic liver disease suggesting a possible link between chronic inflammation and hepatocarcinogenesis.
Authors: Luis E Gomez-Quiroz; Daekwan Seo; Yun-Han Lee; Mitsuteru Kitade; Timo Gaiser; Matthew Gillen; Seung-Bum Lee; Ma Concepcion Gutierrez-Ruiz; Elizabeth A Conner; Valentina M Factor; Snorri S Thorgeirsson; Jens U Marquardt Journal: Toxicology Date: 2016-07-06 Impact factor: 4.221
Authors: Lauren M Aleksunes; Angela L Slitt; Jonathan M Maher; Matthew Z Dieter; Tamara R Knight; Michael Goedken; Nathan J Cherrington; Jefferson Y Chan; Curtis D Klaassen; José E Manautou Journal: Cell Stress Chaperones Date: 2006 Impact factor: 3.667
Authors: Linnea M Baudhuin; Lewis R Roberts; Felicity T B Enders; Russell L Swanson; Teresa A Mettler; Ileana Aderca; Linda M Stadheim; W Edward Highsmith Journal: J Cancer Res Clin Oncol Date: 2005-11-15 Impact factor: 4.553
Authors: Marnie J Wood; Lawrie W Powell; Jeannette L Dixon; V Nathan Subramaniam; Grant A Ramm Journal: World J Gastroenterol Date: 2013-12-28 Impact factor: 5.742