Pathophysiological basis for antioxidant therapy in chronic liver disease

被引:159
作者
Medina, J [1 ]
Moreno-Otero, R [1 ]
机构
[1] Univ Autonoma Madrid, Hosp Univ Princesa, Unidad Hepatol Planta 3, E-28006 Madrid, Spain
关键词
D O I
10.2165/00003495-200565170-00003
中图分类号
R9 [药学];
学科分类号
1007 [药学];
摘要
Oxidative stress is a common pathogenetic mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Cell damage occurs when there is an excess of reactive species derived from oxygen and nitrogen, or a defect of antioxidant molecules. Experimental research on the delicately regulated molecular strategies whereby cells control the balance between oxidant and antioxidant molecules has progressed in recent years. On the basis of this evidence, antioxidants represent a logical therapeutic strategy for the treatment of chronic liver disease. Clinical studies with large numbers of patients have not yet been performed. However, results from several pilot trials support this concept and indicate that it may be worth performing multicentre studies, particularly combining antioxidants with anti-inflammatory and/or antiviral therapy. Oxidative stress plays a pathogenetic role in liver diseases such as alcoholic liver disease, chronic viral hepatitis, autoimmune liver diseases and non-alcoholic steatohepatitis. The use of antioxidants (e.g. S-adenosylmethionine [SAMe; ademetionine], tocopherol [vitamin E], polyenylphosphatidylcholine or silymarin) has already shown promising results in some of these pathologies.
引用
收藏
页码:2445 / 2461
页数:17
相关论文
共 137 条
[51]
Alcohol and mitochondria: A dysfunctional relationship [J].
Hoek, JB ;
Cahill, A ;
Pastorino, JG .
GASTROENTEROLOGY, 2002, 122 (07) :2049-2063
[52]
Hepatocellular carcinoma: Summary and recommendations [J].
Hoofnagle, JH .
GASTROENTEROLOGY, 2004, 127 (05) :S319-S323
[53]
A pilot study of the effects of d-alpha-tocopherol on hepatic stellate cell activation in chronic hepatitis C [J].
Houglum, K ;
Venkataramani, A ;
Lyche, K ;
Chojkier, M .
GASTROENTEROLOGY, 1997, 113 (04) :1069-1073
[54]
[55]
Forum - Mechanisms of hepatotoxicity [J].
Jaeschke, H ;
Gores, GJ ;
Cederbaum, AI ;
Hinson, JA ;
Pessayre, D ;
Lemasters, JJ .
TOXICOLOGICAL SCIENCES, 2002, 65 (02) :166-176
[56]
Oxidative damage is increased in human liver tissue adjacent to hepatocellular carcinoma [J].
Jüngst, C ;
Cheng, B ;
Gehrke, R ;
Schmitz, V ;
Nischalke, HD ;
Ramakers, J ;
Schramel, P ;
Schirmacher, P ;
Sauerbruch, T ;
Caselmann, WH .
HEPATOLOGY, 2004, 39 (06) :1663-1672
[57]
Kageyama F, 2000, AM J GASTROENTEROL, V95, P1041, DOI 10.1111/j.1572-0241.2000.01979.x
[58]
Idiosyncratic drug hepatotoxicity [J].
Kaplowitz, N .
NATURE REVIEWS DRUG DISCOVERY, 2005, 4 (06) :489-499
[59]
Analysis of a form of oxidative DNA damage, 8-hydroxy-2′-deoxyguanosine, as a marker of cellular oxidative stress during carcinogenesis [J].
Kasai, H .
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 1997, 387 (03) :147-163
[60]
EVIDENCE FOR NITRIC OXIDE-MEDIATED OXIDATIVE DAMAGE IN CHRONIC INFLAMMATION - NITROTYROSINE IN SERUM AND SYNOVIAL-FLUID FROM RHEUMATOID PATIENTS [J].
KAUR, H ;
HALLIWELL, B .
FEBS LETTERS, 1994, 350 (01) :9-12