Hepatic oxidative stress and related defenses during treatment of mice with acetylsalicylic acid and other peroxisome proliferators
作者:
Yanong Cai,
Eeva‐Liisa Appelkvist,
Joseph W. Depierre,
期刊:
Journal of Biochemical Toxicology
(WILEY Available online 1995)
卷期:
Volume 10,
issue 2
页码: 87-94
ISSN:0887-2082
年代: 1995
DOI:10.1002/jbt.2570100205
出版商: Wiley Subscription Services, Inc., A Wiley Company
关键词: Oxidative Stress;Peroxisome Proliferators;Lipid Peroxidation;Aminotriazole;Mouse Liver;Antioxidant Defenses
数据来源: WILEY
摘要:
AbstractThe peroxisome proliferators perfluorooctanoic acid (PFOA; 0.02% w/w), perfluorodecanoic acid (PFDA; 0.02%, w/w), nafenopin (0.125%, w/w), clofibrate (0.5%, w/w), and acetylsalicylic acid (ASA; 1%, w/w) were administered to male C57 BL/6 mice in their diet for two weeks. Parameters for Fe3+ADP, NADPH or ascorbic acid‐initiated lipid peroxidation in vitro were measured. Approximately a twofold increase in susceptibility to lipid peroxidation was obtained for all the peroxisome proliferators tested. Cotreatment of mice with the peroxisome proliferator ASA (1%, w/w) and a catalase inhibitor, 3‐amino‐1,2,4‐triazole (AT; 0.4%, w/w) for 7 days resulted in little inhibition of peroxisome proliferation, an elevated level of H2O2in vivo, and total inhibition of the increased susceptibility to lipid peroxidation in vitro. No increase in lipid peroxidation in vivo was observed. Certain antioxidant enzymes (DT‐diaphorase, superoxide dismutase, glutathione transferase, glutathione peroxidase, and glutathione reductase) and components (ubiquinone and α‐tocopherol) were also measured. The results showed that there was some induction of these antioxidant enzymes and components by ASA or aminotriazole, except for glutathione peroxidase and superoxide dismutase, which were inhibited. The possible involvement of oxidative stress in the carcinogenicity of peroxisome proliferators
点击下载:
PDF
(822KB)
返 回