Prevention of benzene-induced myelotoxicity by nonsteroidal anti-inflammatory drugs.

Citation data:

Environmental health perspectives, ISSN: 0091-6765, Vol: 82, Page: 57-64

Publication Year:
1989
Usage 27
Abstract Views 27
Captures 3
Readers 3
Citations 16
Citation Indexes 16
Repository URL:
https://jdc.jefferson.edu/bmpfp/49
PMID:
2792051
DOI:
10.1289/ehp.898257
PMCID:
PMC1568138
Author(s):
G. F. Kalf; M. J. Schlosser; J. F. Renz; S. J. Pirozzi
Publisher(s):
Environmental Health Perspectives; National Institute of Environmental Health Sciences.
Tags:
Medicine; Environmental Science; Animals; Anti-Inflammatory Agents; Non-Steroidal; Arachidonic Acids; Benzene; Bone Marrow Diseases; Indomethacin; Macrophages; Male; Mice; Inbred C57BL; Inbred DBA; Micronucleus Tests; Phenol; Phenols; Prostaglandins E; Medical Biochemistry; Medical Molecular Biology
article description
Benzene affects hematopoietic progenitor cells leading to bone marrow depression and genotoxic effects such as micronucleus formation. Progenitor cell proliferation and differentiation are inhibited by prostaglandins produced by macrophages. Administration of benzene to DBA/2 or C57BL/6 mice caused a dose-dependent bone marrow depression and a significant increase in marrow prostaglandin E level and both were prevented by the coadministration of indomethacin and other inhibitors of the cyclooxygenase component of prostaglandin H synthase. Levels of benzene that decreased bone marrow cellularity also caused genotoxic effects measured as increased micronucleated polychromatic erythrocytes in peripheral blood, which was also prevented by the coadministration of indomethacin. These results suggest a possible role for prostaglandin synthase in benzene myelotoxicity; a mechanism by which this might occur is presented.