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Induction of CYP4F3 in white blood cells from benzene-poisoning patients and human HL60 cells.
Zhao-Z; Mao-Z; Bi-Y; Xia-Y; Tao-N; Li-L; He-X; Ma-Q
17th International Symposium on Microsomes and Drug Oxidations, Saratoga Springs, New York, USA, July 6-10, 2008. Kaminsky LS, ed., Bologna, Italy: Medimond S.r.l., 2008 Jul; :103-107
Exposure to benzene elicits a range of hematotoxicity from leukopenia to leukemia. We used microarray to analyze differential gene expression in the white blood cells (WBC) from 7 patients diagnosed with occupational benzene poisoning compared with 7 matched controls. All patients exhibited elevated expression of CYP4F3, a leukotriene B4 (LTB4) omega-hydroxylase critical in the inactivation of LTB4 in polymorphonuclear leukocytes (PMN), with the fold of induction between 3 and 71. CYP4F3 was also induced in cultured promyolocytic leukemia cells (HL-60) by a benzene metabolite, phenol, similarly to all-trans retinoic acid (ATRA). Induction of CYP4F3 may playa role in benzene hematotoxicity and serve as a biomarker of benzene exposure and toxicity.
Benzenes; Benzene-poisoning; Hematopoietic-system; Blood-disorders; Biomarkers; Solvents
17th International Symposium on Microsomes and Drug Oxidations, Saratoga Springs, New York, USA, July 6-10, 2008
Page last reviewed: March 11, 2019
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