XPD expression and its effect on methylation on Benzene-induced blood toxicity
DOI:
https://doi.org/10.52547/vnz28561Keywords:
Benzene; Hydroquinone; Xeroderma pigmentosum complementation group D; methylationAbstract
Benzene is a known carcinogen that mostly targets and affects the hematopoietic system. It may cause a reduction of whole blood cells, aplastic anemia or even leukemia. To understand the molecular mechanisms of benzene-induced blood toxicity, the epigenetic changes of a deoxyribonucleic acid (DNA) repair gene, Xeroderma pigmentosum complementation group D (XPD), were investigated. Sprague-Dawley (SD) rats and K562 cells were exposed to different concentrations of benzene and its metabolite, hydroquinone. The results showed that both compounds may lead to DNA damage in a dose-dependent manner. Moreover, when their exposure reached a certain dose and time, the expression of XPD messenger ribonucleic acid (mRNA) and protein level increased. Measurement of the methylation status of the XPD gene promoter region in exposed cells revealed that the methylation rate of the XPD gene among groups did not differ significantly. The results of the present study suggested that the changes in XPD mRNA expression and protein level induced by exposure to benzene and its metabolite hydroquinone were not attributed to the abnormal methylation of the XPD gene.
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