Journal Article

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James M. Mathews, Amy S. Etheridge and H. B. Matthews

in Toxicological Sciences

Volume 44, issue 1, pages 14-21
Published in print July 1998 | ISSN: 1096-6080
Published online July 1998 | e-ISSN: 1096-0929 | DOI: http://dx.doi.org/10.1093/toxsci/44.1.14
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The disposition of oral doses of [14C]benzene was investigated using a range of doses that included lower levels (0.02 and 0.1 mg/kg) than have been studied previously in rat, mouse, and in hamster, a species which has not been previously examined for its capacity to metabolize benzene. Saturation of metabolism of benzene was apparent as the dose increased, and a considerable percentage of the highest doses (100 mg/kg) was exhaled unchanged. Most of the remainder of the radioactivity was excreted as metabolites in urine, and significant metabolite-specific changes occurred as a function of dose and species. Phenyl sulfate was the predominant metabolite in rat urine at all dose levels (64–73%) of urinary radioactivity), followed by prephenylmercapturic acid (10–11%). Phenyl sulfate (24–32%) and hydroquinone glucuronide (27–29%) were the predominant metabolites formed by mice. Mice produced considerably more muconic add (15%), which is derived from the toxic metabolite muconaldehyde, than did rats (7%) at a dose of 0.1 mg/kg. Unlike both rats and mice, hydroquinone glucuronide (24–29%) and muconic acid (19–31%) were the primary urinary metabolites formed by hamsters. Two metabolites not previously detected in the urine of rats or mice after single doses, 1,2,4-trihydroxybenzene and catechol sulfate, were found in hamster urine. These data indicate that hamsters metabolize benzene to more highly oxidized, toxic products than do rats or mice.

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Subjects: Medical Toxicology ; Toxicology (Non-medical)

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