Cellular glutathione in fatty liver in vitro models
| Autor: | Martha C. Garcia, Thomas J. Flynn, Margaret Amankwa-Sakyi |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Male
Lipid Peroxides Palmitic Acid Biology Toxicology medicine.disease_cause Models Biological Lipid peroxidation Palmitic acid chemistry.chemical_compound medicine Humans Dose-Response Relationship Drug Fatty liver Hep G2 Cells General Medicine Glutathione Middle Aged medicine.disease Fatty Liver Oxidative Stress Biochemistry chemistry Lipotoxicity Hepatocytes Female Lipid Peroxidation Steatohepatitis Steatosis Oxidative stress Oleic Acid |
| Zdroj: | Toxicology in Vitro. 25:1501-1506 |
| ISSN: | 0887-2333 |
| Popis: | The range of non-alcoholic fatty liver disease (NAFLD) includes simple hepatic steatosis, the inflammatory non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. The accumulation of specific lipids in hepatocytes has been associated with oxidative stress and progression of the disease. Elevated serum free fatty acids and hepatocyte lipotoxicity can be studied in an in vitro cellular model. For this purpose, we cultured the human liver cell line, HepG2/C3A, in medium supplemented with increasing amounts of oleic acid (C18:1) and evaluated oxidative stress by measuring the content of the cellular antioxidant, glutathione (GSH). We observed a dose-dependent steatosis, as determined by Nile Red staining, with concurrent increases of GSH; similar findings were also observed in cultured human hepatocytes. Cells cultured with palmitic acid (C16:0) or the combination oleic/palmitic acids (2:1 ratio) also exhibited a dose-dependent increase of GSH; however palmitic-supplemented cultures did not sustain the GSH increase after 24h. We also detected an increase in the formation of lipid peroxides (LPO) indicating that the increase of GSH was a cellular mechanism that may be related to the high exposure of fatty acids. The results of this in vitro study suggest an antioxidant response against fat overloading and indicate potential differences in response to specific fatty acid-induced hepatic steatosis and associated lipotoxicity. |
| Databáze: | OpenAIRE |
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