The role of lipid peroxidation and glutathione on the glycochenodeoxycholic acid-induced cell death in primary cultured rat hepatocytes.
- Author:
Sang Hui CHU
1
;
Wol Mi PARK
;
Kyung Eun LEE
;
Young Sook PAE
Author Information
1. Department of Pharmacology, College of Medicine, Ewha Womans University, 911-1 Mok-6-dong, Yangchon-gu, Seoul, South Korea.
- Publication Type:Original Article
- Keywords:
Hepatocyte;
Apoptosis;
Glycochenodeoxycholic acid;
Lipid peroxidation;
Glutathione
- MeSH:
Animals;
Apoptosis;
Bile;
Bile Acids and Salts;
Cell Death*;
Cholestasis;
Electrophoresis, Agar Gel;
Glutathione*;
Glycochenodeoxycholic Acid;
Hepatocytes*;
Lipid Peroxidation*;
Liver Diseases;
Necrosis;
Oxygen;
Rats*
- From:The Korean Journal of Physiology and Pharmacology
2000;4(2):121-127
- CountryRepublic of Korea
- Language:English
-
Abstract:
Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver diseases. The objective of this study was to determine the role of lipid peroxidation and glutathione on the bile acid-induced hepatic cell death mechanism in primary cultured rat hepatocytes. To induce hepatic cell death, we incubated primary cultured rat hepatocytes with glycochenodeoxycholic acid (GCDC; 0~400 micrometer) for 3 hours. In electron microscopic examination and agarose gel electrophoresis, low concentration of GCDC treatment mainly induced apoptotic feature. Whereas 400 micrometer GCDC treated cells demonstrated both apoptosis and necrosis. Lipid peroxidation was increased dose-dependently in GCDC treated hepatocyte. And this was also accompanied by decreased glutathione. Therefore, oxygen free radical damage may play a partial role in GCDC-induced hepatic cell death.
