title: Evaluation of redox statuses in patients with hepatitis B virus-associated hepatocellular carcinoma.
abstract: BACKGROUND
  Excess reactive oxygen species related to neoplasia of liver has been established. Essentially, the human body has developed different antioxidant systems for defence against these attacks. To evaluate the redox status in hepatocellular carcinoma (HCC) induced by hepatitis B virus (HBV), the most important aetiological factor in Taiwan, changes in O2(.) generation, lipid peroxidation as well as antioxidant status in the blood of HCC patients with HBV carriers for more than 20 years were measured.
  
  
  METHODS
  Superoxide anion radical (O2(.-)) generation and the levels of malondialdehyde (MDA) served as an index of lipid peroxidation along with the analyses of activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GRx); also, glutathione status, including reduced glutathione (GSH) and oxidized glutathione (GSSG), and the levels of vitamins A, C and E were determined.
  
  
  RESULTS
  In 54 patients, the levels of O2(.-), MDA and GSSG, and the activities of SOD and GRx of blood were significantly higher than those of 57 controls. Conversely, the levels of GSH and total GSH, and GSH/GSSG ratio, and vitamins A and C were significantly decreased. Additionally, there were no significant changes in the activity of GPx and the levels of vitamin E.
  
  
  CONCLUSIONS
  Our data suggest that the redox statuses in patients with HBV-associated HCC were elevated or decreased in certain parameters. However, the increased activities of antioxidant enzymes may be a compensatory up-regulation and the decrease antioxidant statuses were responses to the enhanced oxidative stress in those patients.
authors.affiliation: Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
authors.forename: Shih-Meng
authors.initials: SM
authors.lastname: Tsai
authors.forename: Shu-Kai
authors.initials: SK
authors.lastname: Lin
authors.forename: King-The
authors.initials: KT
authors.lastname: Lee
authors.forename: Jen-Kuei
authors.initials: JK
authors.lastname: Hsiao
authors.forename: Jung-Chih
authors.initials: JC
authors.lastname: Huang
authors.forename: Szu-Hsien
authors.initials: SH
authors.lastname: Wu
authors.forename: Hsu
authors.initials: H
authors.lastname: Ma
authors.forename: Szu-Hwa
authors.initials: SH
authors.lastname: Wu
authors.forename: Li-Yu
authors.initials: LY
authors.lastname: Tsai
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001205:Ascorbic Acid / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000097:blood* / Q000209:etiology* / Q000821:virology; D005260:Female; D005978:Glutathione / Q000097:blood; D019803:Glutathione Disulfide / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D006509:Hepatitis B / Q000150:complications*; D006515:Hepatitis B virus / Q000502:physiology*; D006801:Humans; D008113:Liver Neoplasms / Q000097:blood* / Q000821:virology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010084:Oxidation-Reduction; D013482:Superoxide Dismutase / Q000097:blood; D014801:Vitamin A / Q000097:blood; D014810:Vitamin E / Q000097:blood
chemical_list: D014801:Vitamin A; D014810:Vitamin E; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; D001205:Ascorbic Acid; D019803:Glutathione Disulfide