Abstract
Rainbow trout are known to be more susceptible to aflatoxin B 1 (AFB 1) hepatocarcinogenesis than coho salmon, or trout pre-fed the carcinogenesis inhibitors β-naphthoflavone (βNF), Aroclor 1254 or indole-3-carbinol. The study reported here examined the relationship between AFB 1-glutathione (GSH) conjugation and AFB 1 carcinogenesis in salmon, trout and trout pre-fed the three inhibitors. The AFB 1-glutathione (AFB 1-SG) conjugate was not detected in salmon bile and was present in trout bile in amounts representing less than 0.2% of the administered dose 24 hr after injection of [ 3H]AFB 1. The major conjugates were glucuronides of aflatoxicol and aflatoxicol M 1. In incubations of isolated liver cell fractions, less than 0.5% of the original AFB 1 dose was recovered as AFB 1-SG in salmon and trout preparations, compared to 25% in mouse-liver cell preparations. The GSH concentration in livers of the control trout was higher than that for coho salmon but lower than that for trout pre-fed βNF. Liver GSH-transferase activity in control trout livers was much higher than in the control salmon livers, but was only 62% of that found for trout fed βNF. There was no apparent relationship among the various groups between liver GSH concentration, liver GSH-transferase activity, or biliary GSH conjugate, and the degree of carcinogenic response of AFB 1. Thus current evidence does not indicate a major role for aflatoxin B 1 epoxide-GSH detoxification in coho salmon, or rainbow trout fed any of the three anticarcinogens tested. These results in salmonid fish are contrary to those which suggest AFB 1-SG conjugation as a major determinant of AFB 1 carcinogenesis and its dietary modulation in rodent models.
Published Version
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