AFLATOXIN-B1 AND AFLATOXICOL METABOLISM IN RAINBOW-TROUT (SALMO-GAIRDNERI) AND THE EFFECTS OF DIETARY CYCLOPROPENE

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  • 1 January 1979
    • journal article
    • research article
    • Vol. 2  (3) , 707-718
Abstract
Aflatoxin M1 [AFM1] was identified as a minor metabolite formed by the in vitro incubation of the carcinogen aflatoxin B1 [AFB1] with the postmitochondrial fraction or microsomes from rainbow trout (S. gairdneri) liver. Fresh, whole trout liver converted perfused AFB1 to aflatoxicol [AFL] and AFM1 and converted perfused AFL to AFB1 and AFM1. AFB1 reductive activity was found in the 105,000 xg supernatant, while activity converting AFL to AFB1 was distributed about equally in the 105,000 xg supernatant and in the microsomal pellet. Transformation of AFL to AFB1 was not inhibited by CO, but formation of AFM1 was completely blocked. Cyclopropene fatty acids (CPFA)-fed fish produced only 1/2-1/3 as much AFL from AFB1 as controls, and they produced no detectable AFM1. Most of the untreated AFB1 was recovered by extraction of the incubation medium by organic solvent. In controls, much of it remained bound to the protein. There was no difference in conversion of AFL to AFB1 when results were expressed in terms of postmitochondrial protein levels. CPFA-fed fish had lower microsomal protein and cytochrome P-450 levels and NADPH-cytochrome c reductase and aldrin epoxidation activities than did controls.