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© 1995 Oxford University Press

other

Dehydroepiandrosterone is a complete hepatocarcinogen and potent tumor promoter in the absence of peroxisome proliferation in rainbow trout

Gayle A. Orner 1, Catherine Mathews 2 3, Jerry D. Hendricks 1 2 3, Hillary M. Carpenter 1, George S. Bailey 1 2 3 and David E. Williams 1 2 3 4

1Toxicology Program Oregon State University, Corvallis. OR 97331–6602, USA
2NIEHS Marine/Freshwater Biomedical Sciences Center Oregon State University, Corvallis. OR 97331–6602, USA
3Department of Food Science and Technology Oregon State University, Corvallis. OR 97331–6602, USA

4To whom correspondence should be addressed

Dehydroepiandrosterone (DHEA), fed for 30 weeks to rainbow trout after initiation with the hepatocarcinogen aflatoxin B1 (AFB1), produced a dose-dependent enhancement of carcinogenesis as measured by increased tumor incidence, multiplicity and size. Significant enhancement was observed at 222 p.p.m., which corresponds to a daily dosage one-half that previously administered to humans in clinical trials. DHEA was also capable of acting as a complete carcinogen in this model, producing liver tumors at doses as low as 222–444 p.p.m. Tumors isolated from trout treated with DHEA alone contained mutations in Kims, primarily codon 12[1] G->A transitions, providing the first suggestive evidence that DHEA could be a genotoxic carcinogen. The carcinogenicity of DHEA in trout is independent of peroxisome proliferation, as measurements of peroxisomal (ß-oxidation and catalase activity support previous observations that trout, like humans, are weak respon-ders to peroxisome proliferators.


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