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(4\u20106 times) than with the i.p. route of benzene administration was ruled out as being due to the involvement of gut flora in benzene biotransformation. Pretreatment of males with 3\u2010methylcholanthrene or \u03b2\u2010naphthoflavone, inducers of P\u2010448 monooxygenase, but not phenobarbital, an inducer of P\u2010450, significantly enhanced the myeloclastogenic effect of a single oral dose of benzene (440 mg\/kg). Single oral doses of phenol, catechol, or hydroquinone (250, 150, and 200 mg\/kg, respectively) failed to reproduce the potent myeloclastogenic effect of benzene. In fact, only hydroquinone was mildly clastogenic. The relation between benzene's myeloclastogenicity and metabolism is discussed.<\/jats:p>","DOI":"10.1002\/ajim.4700070511","type":"journal-article","created":{"date-parts":[[2007,4,16]],"date-time":"2007-04-16T04:07:28Z","timestamp":1176696448000},"page":"475-484","source":"Crossref","is-referenced-by-count":23,"title":["Benzene myeloclastogenicity: A function of its metabolism"],"prefix":"10.1002","volume":"7","author":[{"given":"Mohy Morris","family":"Gad\u2010El\u2010Karim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V. M. 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