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ABSTRACT. Zearalenone (ZEA), an estrogenic mycotoxin produced by several Fusarium species, is converted into a more active metabolite, -zearalenol (-ZOL), and a less active metabolite, -zearalenol (-ZOL), by liver subcellular fractions, but evidence of this reaction in other tissues is limited. In order to clarify the role of various tissues in ZEA metabolism in ruminant, we investigated the in vitro metabolic conversion of ZEA by various tissues of adult male and female goats. The results indicate that in the liver, -ZOL was a major metabolite in cytosolic fractions, whereas -ZOL was a predominant metabolite in microsome fractions. Such a feature of ZEA metabolism was confirmed by the K m and V max values from an enzyme kinetics experiment. Post-mitochondrial fractions of the liver converted ZEA predominantly to -ZOL, indicating that the goat liver may function as an activation organ rather than as an inactivation organ, for ZEA metabolism in goats. In most other tissues including rumen tissue, the activity converting ZEA to -ZOL was higher than that to -ZOL. The amount of -ZOL formed by gastrointestinal tissues was 1/8-1/3 of that by the liver tissue in terms of the amount per mg protein, but the contribution of all gastrointestinal tissues to production of -ZOL was estimated to be comparable to that of the liver because of the large mass of gastrointestinal tissues in ruminants. Overall the results show the importance of not only the liver tissue, but also other tissues, especially gastrointestinal ones, in the formation of a potent estrogenic metabolite, -ZOL.

In order to delineate the features of aflatoxin B1 (AFB1) metabolism in various organs of piglets, in vitro metabolism of AFB1 by microsomes and cytosol of the various piglet organs was studied. The AFB1 was converted efficiently to AFP1 by the kidney microsomes. A less efficient metabolism was noted from the AFB1 to AFQ1, AFM1, and aflatoxicol (AFL) in the various organs. The microsomal ability to form AFB1-DNA adduct was higher in liver when compared to the other organs. The cytosolic glutathione-S-transferase activity to convert AFB1-epoxide to AFB1-glutathione conjugate product was relatively higher in the liver and the small intestine. The reductase activity to convert AFB1-dialdehyde to AFB1-dialcohol was similar in all the organs. The results suggest that the variation in susceptibility to the aflatoxin among different organs is attributable mainly to the organ differences in cytochrome P450 activity to form AFB1-epoxide.