NDLI: Long-term exposure of K562 cells to benzene metabolites inhibited erythroid differentiation and elevated methylation in erythroid specific genes

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Toxicology Research Vol - 5 Issue - 4

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Long-term exposure of K562 cells to benzene metabolites inhibited erythroid differentiation and elevated methylation in erythroid specific genes

Content Provider	Royal Society of Chemistry (RSC)
Author	Cui, N. X. Liu, W. J. Jiang, L. Tang, K. Y. Gong, M. Song, W. Wang, Y. Sun, Y. Yu, C. H. Yi, Z. C.
Copyright Year	2016
Abstract	Benzene is a common occupational hazard and a widespread environmental pollutant. Previous studies have revealed that 72 h exposure to benzene metabolites inhibited hemin-induced erythroid differentiation of K562 cells accompanied with elevated methylation in erythroid specific genes. However, little is known about the effects of long-term and low-dose benzene metabolite exposure. In this study, to elucidate the effects of long-term benzene metabolite exposure on erythroid differentiation, K562 cells were treated with low-concentration phenol, hydroquinone and 1,2,4-benzenetriol for at least 3 weeks. After exposure of K562 cells to benzene metabolites, hemin-induced hemoglobin synthesis declined in a concentration- and time-dependent manner, and the hemin-induced expressions of α-, β- and γ-globin genes and heme synthesis enzyme porphobilinogen deaminase were significantly suppressed. Furthermore, when K562 cells were continuously cultured without benzene metabolites for another 20 days after exposure to benzene metabolites for 4 weeks, the decreased erythroid differentiation capabilities still remained stable in hydroquinone- and 1,2,4-benzenetriol-exposed cells, but showed a slow increase in phenol-exposed K562 cells. In addition, methyltransferase inhibitor 5-aza-2′-deoxycytidine significantly blocked benzene metabolites inhibiting hemoglobin synthesis and expression of erythroid genes. Quantitative MassARRAY methylation analysis also confirmed that the exposure to benzene metabolites increased DNA methylation levels at several CpG sites in several erythroid-specific genes and their far-upstream regulatory elements. These results demonstrated that long-term and low-dose exposure to benzene metabolites inhibited the hemin-induced erythroid differentiation of K562 cells, in which DNA methylation played a role through the suppression of erythroid specific genes.
Starting Page	1284
Ending Page	1297
Page Count	14
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	5
Issue Number	5
Journal	Toxicology Research
DOI	10.1039/c6tx00143b
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	CpG site Metabolite Enzyme Enzyme inhibitor Porphobilinogen Hydroquinone Phenol Benzenetriol K562 cells Deoxycytidine Benzene Hemoglobin DNA methylation Methylation
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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