Document Detail

Enhancement of myeloid cell growth by benzene metabolites via the production of active oxygen species.
MedLine Citation:
PMID:  10193577     Owner:  NLM     Status:  MEDLINE    
In low concentrations, benzene and its metabolite hydroquinone are known to have diverse biological effects on cells, including the synergistic stimulation with GM-CSF of hematopoietic colony formation in vitro, stimulation of granulocytic differentiation in vitro and in vivo, and general suppression of hematopoiesis in vivo. These chemicals are also known to be active in the induction of active oxygen species. We used several assays to determine the effects of benzene metabolites (hydroquinone, benzenetriol, benzoquinone) and active oxygen species (xanthine/xanthine oxidase) on cell growth and cell cycle kinetics of the human myeloid cell line HL-60. HL-60 cells treated with these chemicals for 2 h in PBS showed increased growth over untreated controls in a subsequent 18h growth period in complete media. Incorporation of 3H-thymidine was also increased proportionately by these treatments. Catalase treatment abrogated the increased cell growth of all chemicals, suggesting an oxidative mechanism for the effect of all treatments alike. Cell cycle kinetics assays showed that the growth increase was caused by an increased recruitment of cells from G0/G1 to S-phase for both hydroquinone and active oxygen, rather than a decrease in the length of the cell cycle. Benzene metabolite's enhancement of growth of myeloid cells through an active oxygen mechanism may be involved in a number of aspects of benzene toxicity, including enhanced granulocytic growth and differentiation, stimulation of GM-CSF-induced colony formation, apoptosis inhibition, and stimulation of progenitor cell mitogenesis in the bone marrow. These effects in sum may be involved in the benzene-induced "promotion" of a clonal cell population to the fully leukemic state.
J Wiemels; M T Smith
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Free radical research     Volume:  30     ISSN:  1071-5762     ISO Abbreviation:  Free Radic. Res.     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-06-14     Completed Date:  1999-06-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9423872     Medline TA:  Free Radic Res     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  93-103     Citation Subset:  IM    
Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley 94720-7360, USA.
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MeSH Terms
Benzene / metabolism*
Benzoquinones / antagonists & inhibitors,  pharmacology
Catalase / metabolism
Cell Cycle / drug effects
Cell Division / drug effects*
DNA / biosynthesis
Dose-Response Relationship, Drug
Flow Cytometry
HL-60 Cells
Hydroquinones / antagonists & inhibitors,  pharmacology*
Oxygen / metabolism
Reactive Oxygen Species / metabolism*
Time Factors
Xanthine / metabolism
Xanthine Oxidase / metabolism
Reg. No./Substance:
0/Benzoquinones; 0/Hydroquinones; 0/Reactive Oxygen Species; 106-51-4/benzoquinone; 123-31-9/hydroquinone; 533-73-3/hydroxyhydroquinone; 69-89-6/Xanthine; 71-43-2/Benzene; 7782-44-7/Oxygen; 9007-49-2/DNA; EC; EC Oxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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