Influence of naringin on ferric iron induced oxidative damage in vitro
| Autor: | Tiyyagura Koti Reddy, Rajendra Kedlaya, Ganesh Chandra Jagetia, Venkatasubbaiah A. Venkatesha |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Antioxidant
DNA Repair Cell Survival DNA damage medicine.medical_treatment Clinical Biochemistry medicine.disease_cause Ferric Compounds Thiobarbituric Acid Reactive Substances Biochemistry Antioxidants Cell Line Colony-Forming Units Assay Lipid peroxidation Superoxide dismutase chemistry.chemical_compound medicine Humans Naringin Cells Cultured chemistry.chemical_classification biology Superoxide Dismutase Glutathione peroxidase Biochemistry (medical) Hydrogen Peroxide General Medicine Glutathione Oxidants Oxidative Stress Liver chemistry Flavanones biology.protein Oxidation-Reduction Oxidative stress DNA Damage |
| Zdroj: | Clinica Chimica Acta. 347:189-197 |
| ISSN: | 0009-8981 |
| DOI: | 10.1016/j.cccn.2004.04.022 |
| Popis: | Background: Iron is essential for oxygen transport and a variety of cellular processes like respiration and DNA synthesis. It may become toxic when not handled carefully by cellular proteins and shielded from surrounding media. Naringin treatment may help to overcome the iron-induced toxic effects in vitro. Methods: HepG2 cells were treated with 0.5, 1, 2.5, and 5 mmol/ l naringin 1 h before exposure to 0.1, 0.25, 0.5, and 1 mmol/l ferric iron. The effect of iron or naringin or their combination treatment was studied on cell survival, DNA double-strand break induction, DNA oxidation, lipid peroxidation, and various antioxidants. Results: The exposure of cells to iron caused a dose-dependent decline in their clonogenic potential, while naringin pretreatment resulted in a significant elevation in the cell survival. Exposure of cells to iron resulted in a timedependent elevation in DNA strand breaks and a peak level of DNA strand breaks was observed at 24 h, while naringin pretreatment inhibited the DNA double-strand breaks accompanied by an early repair. Similarly, treatment of HepG2 cells with iron caused increased DNA oxidation that showed reduction when cells were pretreated with naringin. The iron overload caused a significant elevation in the lipid peroxidation accompanied by depletion in glutathione (GSH) concentration, while naringin inhibited lipid peroxidation and arrested the iron-induced depletion in the GSH concentration. Iron treatment also reduced various antioxidant enzymes like glutathione peroxidase (GSHPx), catalase, and superoxide dismutase (SOD). Pretreatment of HepG2 cells with naringin resulted in an elevation in all the antioxidant enzymes. Conclusions: Enhanced antioxidant status by naringin could compensate the oxidative stress and may facilitate an early recovery from iron-induced genomic insult in vitro. D 2004 Elsevier B.V. All rights reserved. |
| Databáze: | OpenAIRE |
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