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Twenty-one-day-old rainbow trout Salmo gairdneri embryos were exposed to static solutions of aflatoxin B, (AFB,) (0.5 pprn for 30 min) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (50 ppm for 60 min) to initiate neoplasms of the liver (AFB1 and MNNG) and other organs (MNNG). Ten weeks after the onset of feeding (14 wk after carcinogen exposure) the fish were started on diets containing 500 pprn beta-naphthoflavone (BNF), 1000 pprn phenobarbital (PB), 100 pprn p,pf-dichlorodiphenyltrichloroethane (DDT), 1000 pprn indole-3-carbinol (I3C), or 20 pprn 17-beta-estradiol (E,), (AFB1-exposed fish) or PB, DDT and E2 (MNNG-exposed fish) and fed until the experiment was terminated 12mo after embryo exposure. E2 was a significant enhancer of both AFB, and MNNG hepatocarcinogenesis. I3C, DDT and BNF also enhanced carcinogenesis to a lesser degree, and PB had no effect. Dietary BNF. PB and E2 reduced the growth rate, while DDT, BNF and E2 caused elevated mortalities. E2 appears to have powerful enhancing or promoting properties on trout liver carcinogenesis, an observation that is consistent with elevated incidence5 of experimentally initiated hepatic neoplasms seen in sexually mature female salmonids.

diseases of aquatic organisms

Enhancement of aflatoxin B1 and N-methyl-N'-nitro-N-nitrosoguanidine hepatocarcinogenesis in rainbow trout Salmo gairdneri by 17-B-estradiol and other organic chemicals