Superoxide dismutase in patients with chronic hepatitis C virus infection

被引:99
作者
Larrea, E
Beloqui, O
Muñoz-Navas, MA
Civeira, MP
Prieto, J
机构
[1] Univ Navarra, Dept Internal Med, Pamplona, Spain
[2] Univ Navarra, Liver Unit, Pamplona, Spain
关键词
superoxide-dismutase; PCR; oxidative stress; TNF alpha; hepatitis C virus genotypes; viral load; free radicals;
D O I
10.1016/S0891-5849(97)00437-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It has been reported that hepatitis C virus (HCV) may cause oxidative stress in infected cells. Patients with chronic hepatitis C exhibit an increased production of tumor necrosis factor-alpha (TNF alpha), a cytokine that can produce oxidative stress by stimulating the generation of reactive oxygen; species (ROS). Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme. To investigate cell defense against oxidative stress in HCV infection, we analyzed Mn-SOD mRNA in liver and in peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis C. Mn-SOD expression in PBMC was significantly increased in patients with HCV infection. Patients with sustained virological and biochemical response after therapy showed significantly lower Mn-SOD than patients with positive viremia. By contrast, Mn-SOD expression was not enhanced in the liver of patients with chronic hepatitis C. The values of Mn-SOD mRNA did not correlate with TNF alpha mRNA expression, viral load, or liver disease activity. Our results indicate that in HCV infection an induction of Mn-SOD was present in PBMC but absent in the liver, suggesting that this organ could be less protected against oxidative damage. Oxidative stress could participate in the pathogenesis of HCV infection. (C) 1998 Elsevier Science Inc.
引用
收藏
页码:1235 / 1241
页数:7
相关论文
共 37 条
[1]   INCREASED LEVELS OF OXIDIZED GLUTATHIONE IN CD4(+) LYMPHOCYTES ASSOCIATED WITH DISTURBED INTRACELLULAR REDOX BALANCE IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION [J].
AUKRUST, P ;
SVARDAL, AM ;
MULLER, F ;
LUNDEN, B ;
BERGE, RK ;
UELAND, PM ;
FROLAND, SS .
BLOOD, 1995, 86 (01) :258-267
[2]   N-ACETYL CYSTEINE ENHANCES THE RESPONSE TO INTERFERON-ALPHA IN CHRONIC HEPATITIS-C - A PILOT-STUDY [J].
BELOQUI, O ;
PRIETO, J ;
SUAREZ, M ;
GIL, B ;
QIAN, CH ;
GARCIA, N ;
CIVEIRA, MP .
JOURNAL OF INTERFERON RESEARCH, 1993, 13 (04) :279-282
[3]  
Boveris A., 1982, Free Radicals in Bi%20gy, V5, P65
[4]   EXPOSURE OF CELLS TO NONLETHAL CONCENTRATIONS OF HYDROGEN-PEROXIDE INDUCES DEGENERATION-REPAIR MECHANISMS INVOLVING LYSOSOMAL DESTABILIZATION [J].
BRUNK, UT ;
ZHANG, H ;
DALEN, H ;
OLLINGER, K .
FREE RADICAL BIOLOGY AND MEDICINE, 1995, 19 (06) :813-822
[5]   TRANSFORMING GROWTH FACTOR-BETA-1 AND FACTOR-ALPHA IN CHRONIC LIVER-DISEASE - EFFECTS OF INTERFERON ALFA THERAPY [J].
CASTILLA, A ;
PRIETO, J ;
FAUSTO, N .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 324 (14) :933-940
[6]  
CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
[7]   Association between reactive oxygen species and disease activity in chronic hepatitis C [J].
DeMaria, N ;
Colantoni, A ;
Fagiuoli, S ;
Liu, GJ ;
Rogers, BK ;
Farinati, F ;
VanThiel, DH ;
Floyd, RA .
FREE RADICAL BIOLOGY AND MEDICINE, 1996, 21 (03) :291-295
[8]   IRON STORAGE, LIPID-PEROXIDATION AND GLUTATHIONE TURNOVER IN CHRONIC ANTI-HCV POSITIVE HEPATITIS [J].
FARINATI, F ;
CARDIN, R ;
DEMARIA, N ;
DELLALIBERA, G ;
MARAFIN, C ;
LECIS, E ;
BURRA, P ;
FLOREANI, A ;
CECCHETTO, A ;
NACCARATO, R .
JOURNAL OF HEPATOLOGY, 1995, 22 (04) :449-456
[9]  
FREEMAN BA, 1982, LAB INVEST, V47, P412
[10]  
GIL B, 1993, HEPATOLOGY, V18, P1050