Intracellular Ca2+ Chelators Prevent Dna Damage And Protect Hepatoma 1Clc7 Cells From Quinone-Induced Cell Killing |
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Authors: | J M Dypbukt H Thor P Nicotera |
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Institution: |
a Department of Toxicology, Kurolinska Institute, Stockholm, Sweden |
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Abstract: | Exposure of hepatoma lclc7 cells to 2,3-drniethoxy-1.4-naphthoquinone (DMNQ) resulted in a sustained elevation of cytosolic Ca2+. DNA single strand breaks and cell killing. DNA single strand break formation was prevented when cells were preloaded with either of the intracellular Ca2+ chelators. Quin 2 or BAPTA, to buffer the increase in cytosolic Ca2+ concentration induced by the quinone. DMNQ caused marked NAD+ depletion which was prevented when cells were preincubated with 3-aminobenzamide. an inhibitor of nuclear poly-(ADP-ribose)-synthetase activity. or with either of the two Ca2+ chelators. However. 3-aminobenzamide did not protect the hepatoma cells from loss of viability. Our results indicate that quinone-induced DNA damage. NAD+ depletion and cell killing are mediated by a sustained elevation of cytosolic Ca2+ |
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Keywords: | Cytosolic Ca2 quinone oxidative stress DNA poly-(ADP)-rybosylation ATP |
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