Lovastatin prevents bleomycin-induced DNA damage to HepG2 cells
| Autor: | Mahmoud Etebari, Marjan Nasiri, Shahla Moradi, Abbas Jafarian-Dehkordi |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
DNA damage Bleomycin medicine.disease_cause 03 medical and health sciences chemistry.chemical_compound Pharmacy and materia medica medicine polycyclic compounds bleomycin lovastatin comet assay genotoxicity Lovastatin General Pharmacology Toxicology and Pharmaceutics Hydrogen peroxide Comet assay Superoxide nutritional and metabolic diseases Molecular biology RS1-441 030104 developmental biology chemistry lipids (amino acids peptides and proteins) Original Article Genotoxicity Oxidative stress medicine.drug |
| Zdroj: | Research in Pharmaceutical Sciences Research in Pharmaceutical Sciences, Vol 11, Iss 6, Pp 470-475 (2016) |
| ISSN: | 1735-5362 |
| Popis: | Lovastatin as a member of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors is used as a lipid-lowering agent. It can also inhibit the formation of hydrogen peroxide and superoxide anion and finally leads to decline in oxidative stress processes. Here, we evaluated whether lovastatin can increase DNA damage resistance of HepG2 cells against genotoxicity of the anticancer drug bleomycin (BLM). HepG2 cells were incubated with different concentrations of lovastatin (0.1, 0.5, 1, 5 µM) before exposure to BLM (0.5 µg/mL for one h). The genotoxic dose of BLM and lovastatin was separately determined and comet assay was used to evaluate the genotoxicity. After trapping cells in agarose coated lames, they were lysed and the electrophoresis was done in alkaline pH, then colored and monitored by florescent microscope. The results of this study indicated that lovastatin in doses lower than 5 µM has genoprotective effect and in doses higher than 50 µM is genotoxic. In conclusion, lovastatin is able to protect genotoxic effects of BLM in HepG2 cells. Further studies are needed to elucidate the mechanism(s) involved in this process. |
| Databáze: | OpenAIRE |
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