Chromium-induced genotoxicity and interference in human lymphoblastoid cell (TK6) repair processes

Naouale El-Yamani, Liliana Zuniga, Elitsa Stoyanova, Amadeu Creus, Ricard Marcos

Research output: Contribution to journalArticleResearchpeer-review

13 Citations (Scopus)

Abstract

Two model chromium (Cr) compounds, one hexavalent (sodium chromate) and one trivalent (chromium chloride), were investigated in a human lymphoblastoid cell line (TK6) to increase our knowledge regarding Cr-induced genotoxicity mechanisms. Both selected compounds were genotoxic using the comet assay, although the percentage of DNA in tail obtained after treatment with Cr VI was significantly higher than that obtained with CrIII, at the higher concentrations tested. To determine the nature of the induced damage, enzymes recognizing oxidized bases were used. Treatments with formamidopyrimidine (FPG) and endonuclease III (EndoIII) displayed a greater degree of DNA damage, indicating that the induction of oxidized bases accounts for an important proportion of the damage induced by Cr compounds. In addition, the kinetic repair studies showed that generated DNA damage is removed in approximately 8 h, with the damage induced by CrIII being removed/repaired more rapidly than damage produced by CrVI. To detect Cr interferences with the repair process, a post-treatment was applied after exposure to 2 Gy gamma radiation. Post-treatment significantly delayed the repair kinetics of DNA damage induced by radiation. This interference effect induced by CrVI was more pronounced. In conclusion, evidence indicates that a high proportion of the Cr-induced DNA damage is correlated with oxidative damage, and that both Cr compounds interfere with repair mechanisms involved in repair of DNA damage induced by gamma radiation. Copyright © Taylor & Francis Group, LLC.
Original languageEnglish
Pages (from-to)1030-1039
JournalJournal of Toxicology and Environmental Health - Part A: Current Issues
Volume74
Issue number15-16
DOIs
Publication statusPublished - 1 Aug 2011

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