The effects of sodium diethyldithiocarbamate in fibroblasts V79 cells in relation to cytotoxicity, antioxidative enzymes, glutathione, and apoptosis
| Autor: | Iwonna Rahden-Staroń, Maria Szumiło, Tomasz Grzela, Dagmara Kurpios-Piec, Hanna Czeczot, Emilia Grosicka-Maciąg |
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| Rok vydání: | 2012 |
| Předmět: |
Programmed cell death
Antioxidant Cell Survival Health Toxicology and Mutagenesis medicine.medical_treatment TBARS Apoptosis DNA Fragmentation Toxicology Protein oxidation medicine.disease_cause Thiobarbituric Acid Reactive Substances Antioxidative enzymes Antioxidants Cell Line Protein Carbonylation Lipid peroxidation chemistry.chemical_compound V79 cells Molecular Toxicology Cricetinae Disulfiram In Situ Nick-End Labeling GSH medicine Animals Annexin A5 Coloring Agents Cell Proliferation Glutathione Peroxidase Chemistry Trypan Blue General Medicine Glutathione Fibroblasts Catalase Glutathione Reductase Biochemistry Colorimetry PC Lipid Peroxidation Ditiocarb Oxidative stress |
| Zdroj: | Archives of Toxicology |
| ISSN: | 1432-0738 0340-5761 |
| Popis: | Sodium diethyldithiocarbamate (DETC) is the main metabolite of disulfiram. Recently, we reported that mechanism of disulfiram cytotoxicity in V79 cells might be partially connected with thiol redox-state imbalance. Here, we examined the effect of DETC on the level of intracellular glutathione (GSH), protein oxidation (measured as PC—protein carbonyl content), lipid peroxidation (measured as TBARS—thiobarbituric acid reactive substances), antioxidant enzymatic defense, as well as on apoptosis. We used V79 Chinese hamster fibroblasts cells with and without modulated glutathione (GSH) level by N-acetyl-l-cysteine (NAC). We showed that treatment with DETC at concentrations that cause a moderate increase in thiol-state imbalance but not cell death stimulates oxidative stress measured as increased level of PC and TBARS, adaptive response of GSH-related enzymes and apoptosis. Our results show that cellular effects of DETC are partially attributable to the initial redox cellular state, since the increase of GSH level by NAC pre-treatment prevented the observed changes. |
| Databáze: | OpenAIRE |
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