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Accession number;05A0313188
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| Title;Oxidative Stress in Drug-induced Liver Injury |
| Author;
MAEDA NAOTO
(Tottori Univ., Fac. of Med.)
MURAWAKI YOSHIKAZU
(Tottori Univ., Fac. of Med.)
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Journal Title;Japanese Journal of Intensive Care Medicine
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Journal Code:Z0581B
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ISSN:0389-1194
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VOL.29;NO.2;PAGE.109-116(2005)
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| Figure&Table&Reference;FIG.3, REF.29 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Reactive oxygen species (ROS) are constantly produced in human beings under normal circumstances. Antioxidant systems help to defend the body against ROS but may be overwhelmed during periods of oxidative stress, which leads to cell damage. The liver performs a substantial number of vital metabolic functions and is the main organ for drug and xenobiotic metabolism. Acetaminophen (AAP) overdose can cause severe hepatotoxicity, in which liver injury is initiated by the metabolism of AAP to a reactive metabolite. Carbon tetrachloride (CCl4)-induced hepatic injury originates through the free radical reactions to the metabolism of CCl4 in the liver and sequent initiation of lipid peroxidation. Thus, ROS play an important role in the development of drug-induced hepatic injury. Recently, the number of cases with drug-induced liver injury has been increasing, parallel to the growing number of drugs including health food and 'natural' foods. Further clarifying the role of oxidative stress in drug hepatotoxicity is needed for useful therapy of drug-induced liver injury, and many drugs and treatments now being investigated are directed toward preventing the damage from oxidative stress. (author abst.) |
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