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Food Chem Toxicol ; 135: 110900, 2020 Jan.
Article in English | MEDLINE | ID: mdl-31654710

ABSTRACT

We aimed to study the effect of vanadium(V) exposure on cell viability, nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) and to elucidate if these effects can be reverted by co-exposure to V and manganese (Mn). HepG2 cells were incubated with various concentrations of bis(maltolato)oxovanadium(IV) or MnCl2 for 32 h for viability study. The higher concentrations (59   µM V, 54 nM Mn and 59   µM V+54 nM Mn) were used to study DNA damage and uptake of V and Mn. Comet assay was used for the study of nDNA damage; mtDNA damage was studied by determining deletions and number of copies of the ND1/ND4 mtDNA region. Cellular content of V and Mn was determined using ICPMS. Cellular exposure to 59   µM V decreased viability (14%) and damaged nDNA and mtDNA. This effect was partially prevented by the co-exposure to V + Mn. Exposure to V increased the cellular content of V and Mn (812.3% and 153.5%, respectively). Exposure to Mn decreased the content of V and Mn (62% and 56%, respectively). Exposure to V + Mn increased V (261%) and decreased Mn (56%) content. The positive effects on cell viability and DNA damage when incubated with V + Mn could be due to the Mn-mediated inhibition of V uptake.


Subject(s)
Cell Nucleus/drug effects , Chlorides/pharmacology , DNA Damage/drug effects , Manganese Compounds/pharmacology , Mitochondria/drug effects , Protective Agents/pharmacology , Pyrones/toxicity , Vanadates/toxicity , Cell Survival/drug effects , DNA, Mitochondrial/metabolism , Hep G2 Cells , Humans
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