4.7 Article

Clastogenicity and Aneugenicity of 1,4-Benzoquinone in Different Lineages of Mouse Hematopoietic Stem/Progenitor Cells

Journal

TOXICS
Volume 9, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/toxics9050107

Keywords

benzene; 1,4-benzoquinone; hematopoietic stem/progenitor cells; lineages; chromosomal aberration; Robertsonian translocation

Funding

  1. Ministry of Higher Education, Malaysia [number-FRGS/1/2011/SKK/UKM/03/8]

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The study revealed significant clastogenic effects of the benzene metabolite 1,4-benzoquinone (1,4-BQ) on hematopoietic cells, particularly through Robertsonian translocation (Rb). Different cell lineages showed varying percentages of chromosomal aberrations after exposure to different concentrations of 1,4-BQ. Further investigation is warranted to understand the role of lineage specificity in governing the clastogenic and aneugenic effects of 1,4-BQ.
Previous reports on hematotoxicity and leukemogenicity related to benzene exposure highlighted its adverse effects on hematopoiesis. Despite the reported findings, studies concerning the mechanism of benzene affecting chromosomal integrity in lineage-committed hematopoietic stem/progenitor cells (HSPCs) remain unclear. Here, we studied the clastogenicity and aneugenicity of benzene in lineage-committed HSPCs via karyotyping. Isolated mouse bone marrow cells (MBMCs) were exposed to the benzene metabolite 1,4-benzoquinone (1,4-BQ) at 1.25, 2.5, 5, 7, and 12 mu M for 24 h, followed by karyotyping. Then, the chromosomal aberration (CA) in 1,4-BQ-exposed hematopoietic progenitor cells (HPCs) comprising myeloid, Pre-B lymphoid, and erythroid lineages were evaluated following colony-forming cell (CFC) assay. Percentage of CA, predominantly via Robertsonian translocation (Rb), was increased significantly (p < 0.05) in MBMCs and all progenitors at all concentrations. As a comparison, Pre-B lymphoid progenitor demonstrated a significantly higher percentage of CA (p < 0.05) than erythroid progenitor at 1.25, 2.5, and 7 mu M as well as a significantly higher percentage (p < 0.05) than myeloid progenitor at 7 mu M of 1,4-BQ. In conclusion, 1,4-BQ induced CA, particularly via Rb in both MBMCs and HPCs, notably via a lineage-dependent response. The role of lineage specificity in governing the clastogenicity and aneugenicity of 1,4-BQ deserves further investigation.

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