Evaluation of oxidative damage and inhibition of DNA repair in an in vitro study of nickel exposure

It has been suggested that Nickel is involved in oxidative damage and inhibition of DNA repair. We studied the effects of NiSO₄ on oxidative stress and DNA repair in Jurkat cells to elucidate its mechanism of action. Cells were treated with H₂O₂ and ROS generation (by flow cytometry), and oxidative DNA damage (as tail moment by Fpg-enzyme comet test), were evaluated immediately and after 4 and 24 h of DNA damage recovery occurred in presence or absence of NiSO₄ (0.017 and 0.17 μ) to clarify possible interactions of Ni with DNA repair processes. Moreover, cells were exposed to the same doses of NiSO₄ for 4 and 24 hours to evaluate its direct oxidative effect. The results of the comet test showed high tail moment immediately after oxidative burst with a decreasing after 4 h of DNA recovery, and a slight increase after 24 h of recovery. The decreases were more limited for cells treated with NiSO₄ 0.17 μ indicating an inhibition of oxidative DNA damage repair by this substance. An induction of ROS was observed after 4 h of incubation with higher dose of NiSO₄. Cells treated with H₂O₂ showed the highest level of ROS after 4 h of recovery in presence of NiSO₄ 0.17 μ that remained at elevated levels also after 24 h of recovery suggesting a synergistic action of Ni with H₂O₂ in the reduction of cellular anti-oxidative defence activities.