PMID- 15586939
OWN - NLM
STAT- MEDLINE
DCOM- 20050111
LR  - 20190827
IS  - 0009-2797 (Print)
IS  - 0009-2797 (Linking)
VI  - 149
IP  - 2-3
DP  - 2004 Oct 15
TI  - Stimulation of endothelial IL-8 (eIL-8) production and apoptosis by phenolic 
      metabolites of benzene in HL-60 cells and human bone marrow endothelial cells.
PG  - 177-88
AB  - Benzene toxicity is considered to be elicited by its metabolites and phenolic 
      metabolites of benzene are known to induce apoptosis in leukemia cells in culture 
      and in human bone marrow progenitor cells. One potential mechanism of apoptosis 
      induced by benzene metabolites that has not been examined is the production of 
      pro-apoptotic cytokines such as endothelial IL-8 from endothelial cells in bone 
      marrow stroma. In this study, we utilized HL-60 cells which are known to produce 
      the endothelial form of IL-8 (elL-8) and human bone marrow endothelial cells 
      (HBMEC) as model systems. Hydroquinone (HQ), Catechol (Cat) and benzenetriol (BT) 
      all induced eIL-8 production and apoptosis in HL-60 cells. HQ induced a marked 
      50-70-fold stimulation of eIL-8 levels and HL-60 cells were shown to have the 
      eIL-8 receptor, CXCR I thus enabling an autocrine pathway of apoptosis. However, 
      treatment with recombinant elL-8 failed to induce apoptosis in HL-60 cells as 
      previously reported and antibodies to either IL-8 or CXCRI did not significantly 
      abrogate benzene metabolite-induced apoptosis. HQ and Cat but not BT also induced 
      stimulation of elL-8 production in HBMEC. These data demonstrate that although 
      metabolites of benzene induce marked stimulation of eIL-8, this is unlikely to be 
      responsible for apoptosis induced in HL-60 cells. Our data also demonstrates that 
      phenolic metabolites of benzene stimulate the production of eIL-8 from HBMEC 
      suggesting that higher levels of endothelial-derived cytokines may occur in bone 
      marrow after benzene exposure.
FAU - Bironaite, Daiva
AU  - Bironaite D
AD  - Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado 
      Health Sciences Center, 4200 East, 9th Avenue, Denver, CO 80262, USA.
FAU - Siegel, David
AU  - Siegel D
FAU - Moran, Julie L
AU  - Moran JL
FAU - Weksler, Babette B
AU  - Weksler BB
FAU - Ross, David
AU  - Ross D
LA  - eng
GR  - R01 ES09554/ES/NIEHS NIH HHS/United States
PT  - Corrected and Republished Article
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Chem Biol Interact
JT  - Chemico-biological interactions
JID - 0227276
RN  - 0 (Antibodies)
RN  - 0 (Benzene Derivatives)
RN  - 0 (Interleukin-8)
RN  - 0 (Receptors, Interleukin-8A)
RN  - 0 (Recombinant Proteins)
SB  - IM
CRF - Chem Biol Interact. 2004 Aug 10;149(1):37-49. PMID: 15356918
MH  - Antibodies/immunology/pharmacology
MH  - Apoptosis/*drug effects
MH  - Benzene Derivatives/*toxicity
MH  - Bone Marrow Cells/*drug effects/metabolism/pathology
MH  - Cell Survival/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Dose-Response Relationship, Immunologic
MH  - Endothelium, Vascular/*drug effects/metabolism/pathology
MH  - HL-60 Cells
MH  - Humans
MH  - Interleukin-8/*biosynthesis/immunology
MH  - Neutralization Tests
MH  - Receptors, Interleukin-8A/immunology
MH  - Recombinant Proteins/immunology/pharmacology
EDAT- 2004/12/14 09:00
MHDA- 2005/01/12 09:00
CRDT- 2004/12/14 09:00
PHST- 2004/12/14 09:00 [pubmed]
PHST- 2005/01/12 09:00 [medline]
PHST- 2004/12/14 09:00 [entrez]
AID - S0009-2797(04)00127-9 [pii]
AID - 10.1016/j.cbi.2004.09.018 [doi]
PST - ppublish
SO  - Chem Biol Interact. 2004 Oct 15;149(2-3):177-88. doi: 10.1016/j.cbi.2004.09.018.