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Hydroquinone (HQ), a metabolite of benzene, is known to be associated with acute myelogenous leukemia (AML) risk;however, its carcinogenic mechanism remains unclear.We now report that HQ induces DNA damage, as evidenced by H2AX phosphorylation and Comet assay.In this study, we knocked down poly(ADP-ribose) polymerase-1 (PARP-1) expression by using RNA interference in TK6 cells.In PARPl-deficient TK6 cells (TK6-PARP1-sh) the PARP-1 were repressed 83.2%.In the HQ treated TK6 cells, the subsequent activation of the DNA nick sensor enzyme, poly(ADP-ribose) polymerase-1 (PARP-1), leads to the rapid depletion of ATP and NAD.In TK6-PARP 1-sh, HQ-induced caspase-3 activation was reduced, suggesting that PARP-1 participates in caspase-dependent apoptosis.Under hydroquinone (HQ) treatment (2.5-40 uM), TK6-PARP1-sh cells demonstrated more apoptosis than that in TK6.DNMT 1 in TK6-PARP l-sh were lower than that of TK6 cells.We found that DNA methylatransferase 1 (DNMT1) was up-regulated under HQ treatment both in TK6 and TK6-PARP 1-sh, and their mRNA expression was increased accordingly.In summary, HQ-induced apoptosis of TK6 cells is accompanied by PARP-1, caspase activation;Taken together, our data allow further characterization of the features of PARP-1 in DNA repair and bring additional evidence that PARP-1 play a role in DNA methylation.