Effect of copper deficiency on oxidative DNA damage in Jurkat T-lymphocytes

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
George Loo, Professor (Creator)
Institution
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/

Abstract: The micronutrient copper is a catalytic cofactor for copper, zinc superoxide dismutase and ceruloplasmin, which are two important antioxidant enzymes. As such, a lack of copper may promote oxidative stress and damage. The purpose of this study was to determine the effect of copper deficiency on oxidative damage to DNA in Jurkat T-lymphocytes. To induce copper deficiency, cells were incubated for 48 h with 5-20 µM 2,3,2-tetraamine (2,3,2-tet), a high affinity copper chelator. Such treatment did not affect cell proliferation/viability, as assessed by measuring mitochondrial reduction of WST-1 reagent (4-[3-(4-Iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate). Furthermore, the induction of copper deficiency did not promote oxidative DNA damage as evaluated by the comet assay. Comet scores were 15 ± 0 and 16 ± 1 for control and copper-deficient cells, respectively. However, the copper-deficient cells sustained greater oxidative DNA damage than the control cells (comet scores of 175 ± 15 and 50 ± 10, respectively) when both were oxidatively challenged with 50 µM hydrogen peroxide (H2O2), Supplemental copper but not zinc or iron prevented the potentiation of the H2O2-induced oxidative DNA damage caused by 2,3,2-tet. These data suggest that copper deficiency compromises the antioxidant defense system of cells, thereby increasing their susceptibility to oxidative DNA damage.

Additional Information

Publication
Free Radical Biology and Medicine, 28, 824-830.
Language: English
Date: 2000
Keywords
Copper, DNA damage, Jurkat T-lymphocytes, Reactive oxygen species, Free radicals