Benzene myeloclastogenicity: A function of its metabolism

Mohy Morris Gad‐El‐Karim, V. M.Sadagopa Ramanujam, Ahmed E. Ahmed, Marvin S. Legator

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

Using the micronucleus test we have found no significant difference between germ‐free and conventional (non‐germ‐free) male CD‐1 mice gavaged twice with 440 or 880 mg benzene/kg. Hence, the higher myeloclastogenicity observed previously with the p.o. (4‐6 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‐methylcholanthrene or β‐naphthoflavone, inducers of P‐448 monooxygenase, but not phenobarbital, an inducer of P‐450, 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.

Original languageEnglish (US)
Pages (from-to)475-484
Number of pages10
JournalAmerican Journal of Industrial Medicine
Volume7
Issue number5-6
DOIs
StatePublished - 1985

Keywords

  • 3‐methylcholanthrene
  • chromosomal damage
  • hydroquinone
  • micronucleus test in mice
  • mixed function oxidase inducers
  • muconic acid
  • phenobarbital
  • phenol
  • route of administration
  • β‐naphthoflavone

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health

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