Abstract
Isolated hepatocytes from rainbow trout readily activated aflatoxin B1 (AFB1) to mutagens detectable by S. typhimurium TA 98. Characterization studies demonstrated that activation efficiency was essentially linear with respect to hepatocyte concentration (5 X 10(5)-2 X 10(7) cell/ml) and AFB1 dose (0-10 micrograms/ml). This system was employed to assess possible differences in AFB1 activation in hepatocytes from rainbow trout and coho salmon, two species which have been shown in in vivo studies to differ widely in sensitivity to AFB1 carcinogenesis. Activation efficiency was approximately three times greater in trout hepatocytes compared with salmon hepatocytes. This difference was more marked when S20 liver fractions from the two species were used. Analysis of unbound [3H]AFB1 metabolites performed on supernatants of hepatocyte incubations revealed that under the normal conditions of assay, addition of bacteria does not perturb the various pathways of AFB1 metabolism within hepatocytes. These results support other studies which suggest that the greater sensitivity of trout to AFB1 carcinogenicity resides largely in increased initial DNA damage, compared with coho salmon.
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