Benzene-induced cytotoxicity and apoptosis in TrHBMEC and HL-60 cell lines

1 Dept. of Pharmaceutical Sciences, Box C238, School of Pharmacy, UCHSC, 4200 East 9th Ave, Denver, CO, USA 2 Cornell University, Coll. Med., New York, NY 3 Dept. of Developmental Biology, Institute of Biochemistry, Mokslininku 12, 08662 Vilnius, Lithuania Benzene is a ubiquitous pollutant and known human leukemogen. The mechanism(s) by which benzene causes leukemia still remain unknown. It is generally accepted that in order to exert its cytotoxicity, benzene has to be metabolically activated to hydroquinone (HQ), catechol (Cat.), 1, 2, 4-benzenetriol (BT) and phenol (Phe). Both cell lines after the stimulation with benzene metabolites produce eIL-8, which has been reported to have proapoptotic and cytotoxic effects in HL-60 and TrHBMEC lines, respectively. The slight inhibition of apoptosis by catalase, IL-8 and CXCR1 monoclonal antibodies supports the hypothesis about a complex mechanism of cell toxicity, induced apoptosis and possible excitation of leukemia by hydroxylated benzene metabolites.