Effects of Ethanol and Endotoxin on Antioxidant System in Perfused Heart.

• Main Authors: Chin-Shun, Hsu, 許金順
• Other Authors: Shu-Mei, Lin
• Format: Others
• Language: zh-TW
• Published: 2006
• Online Access: http://ndltd.ncl.edu.tw/handle/12699559370856293563

碩士 === 中華醫事學院 === 生物科技研究所 === 92 === Excessive alcohol consumption can cause multiorgans failure. The ethanol-induced heart injury is major known as alcoholic cardiomyopathy, and the mechanism of which is still not completely understood. Oxidative stress is associated with the hepatic injury caused by alcohol, but its role in alcoholic cardiomyopathy is uncertain. Oxidative stress is the condition as result of the imbalance between cellular oxidant generation and antioxidant capacity due to increase in reactive oxygen species, decrease in antioxidants or both. The objective of the present study is to investigate the effect of alcohol on the antioxidant capacity of the heart tissue. Additionally, clinical study demonstrated that serum endotoxin level was increased in alcoholic patients. Therefore, whether endotoxin enhance the alcohol-induced oxidative stress is also studied in an in vitro rat heart perfusion model. The results show that lactate dehydrogenase activity is significantly increased in the heart tissues perfused with 0.5% ethanol, lipopolysaccharide (LPS) alone or co-perfusion with LPS and ethanol, compared with control group. LPS plus ethanol causes more LDH leaked from heart tissue compared with LPS or ethanol alone. Thiobarbituric acid reactive substances (TBARS) level is also significantly higher in ethanol and LPS group compared with control group, but LPS plus ethanol group is significantly decreased than in the tissue perfused ethanol alone. The results from antioxidant enzyme assay suggest that SOD and CAT activities in the heart are significantly increased after perfused with ethanol or LPS＋0.5% ethanol group, but there was no effect on the activities of GPx and GR. In conclusion, this study demonstrated that alcohol and LPS perfusion caused cardiac tissue injury which is concurrent with increased of lipid peroxidation. Co-perfusion with LPS exacerbated alcohol toxicity. Furthermore, SOD and Cat might play critical role in the cellular compensatory response to alcohol. The overall results from this study suggest the involvement of ROS in alcohol cardiotoxicity.