Isolation and identification of dihydrocitrinone, a urinary metabolite of citrinin in rats

Abstract

Dihydrocitrinone, 3,4-dihydro-6,8-dihydroxy-3,4,5-trimethylisocoumarin-7-carboxylic acid, was isolated and identified as a urinary metabolite after oral administration of citrinin to rats. Male and female Osborne-Mendel rats received 30 mg citrinin/kg body weight by oral intubation. The metabolite dihydrocitrinone was present in urine collected at 0-2, 2-4, 4-6, 6-8, and 8-24 h after treatment. Only unchanged citrinin was found in blood collected 24 h after administration of the compound. The metabolite had a blue fluorescence and the same Rf on thin-layer chromatography, the same retention time on reverse-phase high-pressure liquid chromatography, and the same mass spectrum as an authentic sample of dihydrocitrinone.

A direct assessment of mycotoxin biomarkers in human urine samples by liquid chromatography tandem mass spectrometry

“…Literature on the toxicokinetics and metabolism of CIT in humans is very scarce. However, Dunn et al [32] isolated and successfully identified dihydrocitrone as the main urinary metabolite of CIT in rats. Low levels (2-5 ng/mL) of the un-metabolized toxin were also detected in the urine of humans [33], indicating a possible but low level of excretion.…”

Electrochemical simulation of biotransformation reactions of citrinin and dihydroergocristine compared to UV irradiation and Fenton-like reaction

“…It is conceivable that the dealkylation achieved by EC may also take place in biological systems during the enzymatic oxidation of CIT and is of particular importance concerning the poor data conditions of CIT metabolites. Relatively well understood is the CIT-derived metabolite dihydrocitrinone which has been found to be a major metabolite in the urine of rats [21] and humans [22]. Whether the m/z 267 detected by using EC/ESI-MS is dihydrocitrinone needs to be confirmed by structural elucidation.…”

Mycotoxins Affecting the Kidney

“…Berndt and colleagues (Berndt and Hayes, 1982;Berndt, 1983) support the theory that citrinin itself is responsible as no renal metabolism of citrinin could be detected in their investigations. In contrast, the presence of the urinary metabolite dihydrocitrione has been demonstrated (Dunn et al, 1983), however, only 10 to 20% of citrinin is excreted as metabolites hence the possible role in renal toxicity is as yet, unknown.…”