Lack of hepatic microsomal metabolism of deoxynivalenol and its metabolite, DOM-1

L. M. Côté, W. Buck, E. Jeffery

Research output: Contribution to journalArticlepeer-review

Abstract

Rat hepatic microsomal preparations were used to study the metabolism of deoxynivalenol (DON) and its metabolite 3α,7α,15-trihydroxytrichothec-9,12-dien-8-one (DOM-1). The N-demethylation of ethylmorphine was monitored to assess the viability of the mixed-function oxidase. DON was incubated with microsomes and an NADPH-generating system. Samples were removed from the incubation system and analysed for DON using an HPLC equipped with a UV detector. After incubation for 30 min, there was no evidence of disappearance of DON or of the presence of new metabolites; neither was microsomal NADPH oxidation altered by the addition of DON. Rat and pig hepatic microsomal preparations were used to assess DON glucuronidation, using p-nitrophenol disappearance to check the viability of the microsomal glucuronidating system. When DON was incubated with microsomes and 14C-labelled uridine 5′-diphosphoglucuronic acid, no radioactivity was detected in the TLC zone where the glucuronide was expected. Three rats and one pig were dosed orally with 2 mg DON/kg and samples of their urine and faeces were extracted and incubated with β-glucuronidase or with buffer only. No differences in DON or DOM-1 concentrations were detected between samples incubated with or without β-glucuronidase. These results suggest that DON was neither bioactivated to a more toxic product nor oxidized to a less toxic compound by the rat hepatic mixed-function oxidase system. Likewise, DOM-1 was not reactivated or metabolized by this system. Neither DON nor DOM-1 glucuronides were formed either in in vitro liver systems or in vivo.

Original languageEnglish (US)
Pages (from-to)291-295
Number of pages5
JournalFood and Chemical Toxicology
Volume25
Issue number4
DOIs
StatePublished - Apr 1987

ASJC Scopus subject areas

  • Food Science
  • Toxicology

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