Aflatoxicol-induced hepatocellular carcinoma in rainbow trout (Salmo gairdneri) and the synergistic effects of cyclopropenoid fatty acids

• Published in: Cancer research (Chicago, Ill.) Ill.), 1981-03, Vol.41 (3), p.1011-1014
• Main Authors: Schoenhard, G L, Hendricks, J D, Nixon, J E, Lee, D J, Wales, J H, Sinnhuber, R O, Pawlowski, N E
• Format: Article
• Language: English
• Subjects: Aflatoxins - metabolism; Animals; Biotransformation; Drug Synergism; Fatty Acids, Unsaturated; Liver - metabolism; Liver Neoplasms, Experimental - chemically induced; Salmonidae - physiology; Trout - physiology
• ISSN: 0008-5472

Aflatoxicol (AFL), a major metabolite of aflatoxin B1 (AFB1) in the Mt. Shasta rainbow trout (Salmo gairdneri), was found to produce hepatocellular carcinoma in trout. It was administered in a casein diet to duplicate groups of 120 fingering trout. In the same manner, additional duplicate groups received one of the following: no toxicant; AFB1; the diastereomer of AFL (AFL'); cyclopropenoid fatty acids (CPFA); and CPFA plus AFB1, AFL, and AFL'. Eight months after the initiation of the study, the following incidences of carcinoma were observed: control (0%); 20 ppb AFB1 (56%); 29 ppb AFL (26%); 61 ppb AFL' (0%); 50 ppm CPFA (3%); 20 ppb AFB1 plus 50 ppm CPFA (96%); 29 ppb AFL plus 50 ppm CPFA (94%); and 61 ppb AFL' plus 50 ppm CPFA (55%), showing both the carcinogenicity of AFL and the synergistic effects of CPFA. Twelve-month incidences were correspondingly higher in all cases. Aflatoxin M1, another metabolite of AFB1 in rainbow trout, was reported previously to be carcinogenic in trout. These results support the hypothesis that metabolism in rainbow trout does not effectively detoxify AFB1, but rather the formation of AFL extends the carcinogenicity of AFB1 and may contribute to the high sensitivity of rainbow trout to AFB.