Abstract:
:Hydroquinone (HQ), one of the most important metabolites derived from benzene, is known to be associated with acute myelogenous leukemia risk; however, its carcinogenic mechanism remains unclear. In a previous study, we found that low-level of benzene exposure down-regulated the expression of poly(ADP-ribose)polymerase 1 (PARP1). Here, we employed RNA interference to knock down PARP1 expression in TK6 cells and explored the potential role of PARP1 in HQ-induced cytotoxicity. The results showed that stable PARP1-knockdown cells were successfully constructed and more than 80% inhibition of PARP1 expression was confirmed. We found that HQ treatment of TK6 cells decreased cell viability, increased cell apoptosis, and caspase3/7 activity. Knockdown of PARP1 in HQ-treated TK6 cells prevented caspase3 activation, and increased apoptosis than that in the wild-type TK6 cells, with fully functional PARP1. The results also showed that down-regulation of PARP1 led to a decrease in cell proliferation and an enhanced susceptibility to HQ-induced cytotoxicity with concentration less than 40 μM than that in normal TK6 cells. Moreover, PARP1-knockdown TK6 cells treated with HQ displayed an increased level of DNA double-strand breaks as measured by olive tail moment. No evidence was obtained of an effect of PARP1 depletion on H2AX phosphorylation induction. Under the experimental conditions, PARP1 has a role in HQ-induced DNA damage repair rather than in long-term chromatin modifications signaled by phosphorylated H2AX.
journal_name
Toxicol Mech Methodsjournal_title
Toxicology mechanisms and methodsauthors
Sha Y,Zhou W,Yang Z,Zhu X,Yang X,Li TD,Zhu Ddoi
10.3109/15376516.2015.1070222subject
Has Abstractpub_date
2015-01-01 00:00:00pages
467-77issue
6eissn
1537-6516issn
1537-6524journal_volume
25pub_type
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