Skip Navigation
Skip to contents

JPMPH : Journal of Preventive Medicine and Public Health

OPEN ACCESS
SEARCH
Search

Author index

Page Path
HOME > Browse Articles > Author index
Search
Jong Moon Lee 1 Article
The Protective Effects of Garlic against Carbon tetrachloride-induced Hepatotoxicity.
Byung Sun Choi, Jong Moon Lee, Jung Duck Park, Yeon Pyo Hong
Korean J Prev Med. 2002;35(3):221-228.
  • 8,345 View
  • 22 Download
AbstractAbstract PDF
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. METHODS: Male Sprague-Dawley rats received garlic (0.5 %) or regular diet, for 4 weeks. This was followed by a single dose of corn oil (the controls), carbon tetrachloride (400mg/kg body weight) and trichloroethylene (2,000mg/kg body weight) being administered to each diet 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 significantly in the carbon tetrachloride treated group. Conclusions : The results indicate that garlic attenuates the carbon tetrachloride-induced hepatotoxicity, through the prevention of the metabolic activation and lipid peroxidation.
Summary

JPMPH : Journal of Preventive Medicine and Public Health