No abstract

SUMMARYThecovalent bindingof [6, H]ethinylestradiol (EE)and [6,7-3 H]estrone (E) to liver DNA of 200 g female ratswas measured 8 h after the administration of 80 J..Lg (9.2 mCi) estrogen by gavage. The binding is 1.5 for EE and 1.1 for E, expressedas binding to DNA/dose, in units of ~mol hormonefmol DNA phosphate/mmole honnone/kg body wt. It is in the same order of magnitude as for benzene and about 10 000 tim es below the binding of typical liver carcinogens, such as aflatoxin B 1 or N,N-dimethylnitrosamine.

Abstract-Ring-labelled [ 14 C)aftatoxin 8 1 (AFB.), prepared by biosynthesis. or ~enerally Iabeiied [ 3 H]AFB 1 was administered by oral gavage to young adult _male rat~. After 6 hr. ~he hver _w~~ removed and two fractions were isolated, namely macromolecules, wh1ch contamed about 3 /o of the lmtlal dose of AFB 1 radioactivity. and water-soluble. low-molecular aftatoxin conjugates containing about_0·2~~~ of the administered radioactivity. These two fractions were administered orally to other rats ·~ o~der to determine the potential of radioactive aftatoxin residues for covalent binding to DNA. Such b1.n~mg ~an be used as an indicator for carcinogenic potency. Liver DNA was isolated 9-12 hr after admm1strat1on of the aftatoxin derivatives and in no case was any radioactivity detected on the DNA. lt can bt deduced on the basis of the Iimit of detection of radioactivity on the DNA, that macromolecule· bound AFB 1 derivatives are at least 4000 times less active than AFB 1 with respect to covalent binding to rat-liver DNA. and that the water-soluble conjugates are at least 100 times less potent than AFB, itself. 1t is concluded that the carcinogenic risk for humans who consume liver or n:'eat. containing s~h aftatoxin residues is negligible when compared with the risk from intake of aftatoxms m other food 1tems.