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)
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

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

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