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마늘에 의한 사염화탄소 간독성의 보호 효과The Protective Effects of Garlic against Carbon tetrachloride-induced Hepatotoxicity

Authors
최병선이종문박정덕홍연표
Issue Date
Aug-2002
Publisher
대한예방의학회
Keywords
Garlic; Carbon tetrachloride; Trichloroethylene; Liver/injuries; Protective agents
Citation
예방의학회지, v.35, no.3, pp 221 - 228
Pages
8
Journal Title
예방의학회지
Volume
35
Number
3
Start Page
221
End Page
228
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/55477
ISSN
1975-8375
2233-4521
Abstract
Objectives: The purpose of this study was to find the protective effects of garlic on the halogenated hydrocarbon induced hepatotoxicities, and the possible protection mechanisms involved. Melluds Male Sprague-Dawley rats received garlic (0.5%) OF regular diet, for 4 weeks. This was followed by a single dose of com oil (the controls), carbon tetrachloride (400mg/kg body weight) and trichloroethylene (2,000mg/kg body weight) being administered to each del group. Blood samples were collected 24 hours following the administration, and the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities measured. The liver samples were studied for their cytochrome P450 and CYP2E1 contents, lipid peroxidation and histopathology. Results: The results for the group receiving the 0.5% garlic diet showed a slight decrease of CYP2E1 expression compared with the regular diet group. Carbon tetrachloride was significantly decreased the CYP2E1 contents in both the regular and garlic diet groups, but the trichloroethylene remained unchanged. Garlic did not decrease the lipid peroxidation of the liver in the control group, but attenuated the increase of lipid peroxidation caused by carbon tetrachloride, Garlic attenuated the increase of both the serum AST and ALT activities caused by carbon tetrachloride. The histopathological observations also showed that garlic attenuated centrilobular necrosis and vacuolar degenerative changes signincantly in the carbon tetrachionde treated group. Conclusions: The results indicate that garlic attenuates the carbon tetrachloride-induced hepatotoxicity, through the prevention of the metabolic activation and lipid peroxidation.
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