By S. Lekhnitskii, S. W. Tsai, T. Cheron

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P. C . p. p. a S e e also Table V for carcinogenicity studies using feed or aflatoxin mixtures. b M i c e were treated during c 174-181) 190) aflatoxin-contaminated infancy. A c t i v e when used as a tumor-initiator followed by promotion with crotón oil. 4 μπιοΐ/kg AFBj the first day after birth. Parallel studies indicate that female mice are much less susceptible; liver tumors, with an incidence of 7%, were detected only in the group that received AFB! at 7 days of age. Studies in various laboratories (summarized in Table VI) show that purified AFBj is a highly potent hepatocarcinogen in the rat, and clear dose-response relationships have been established (140, 165, 170).

5 mg sterigmatocystin to a group of 6 rats twice weekly for 24 weeks. Local sarcomas were observed in 3 of 6 animals at the end of the 65-week study; no such tumors occurred in control rats. However, sterigmatocystin is ä substantially weaker local carcinogen than AFB, in the rat by the subcutaneous route. Dickens et al. 5-mg dose of sterigmatocystin to be comparable to a 2 ^ g dose of A F B , . Purchase and van der Watt (204) applied 1 mg sterigmatocystin (dissolved in dimethyl sulfoxide or acetone) onto the shaved dorsal skin of male Wistar-derived rats twice weekly for 70 weeks.

Aflatoxin B, binds covalently to nucleic acids after in vitro metabolic activation by liver microsomes (53, 55, 235-239) as well as in in vivo studies (49, 191, 223, 238, 240-243). 2), indicating the involvement of AFB,-2,3oxide. In the absence of exogenous nucleophiles, 2,3-dihydro-2,3-dihydroxyaflatoxin B , , an expected hydrolysis product of AFB,-2,3-oxide, is a major metabolite in the incubation of AFB, with rat, hamster, and trout liver micro­ somes (244-247). An A F B , - G S H conjugate, tentatively identified as 2,3-dihydro-2-(5-glutathionyl)-3-hydroxyaflatoxin B , , was also detected as an in vitro as well as in vivo metabolite of AFB, in the rat.

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