The ability of vitamin C to inhibit induction of renal carcinoma by estrogens was tested in male Syrian hamsters in vivo. The animals received estrogen (estradiol or diethylstilbestrol) implants s.c. Hamsters which were continuously given vitamin C, administered in the drinking water for estradiol-treated or in the food for diethylstilbestrol-treated animals, were observed to develop renal carcinoma with a significantly lower incidence (10 of 33 animals with estradiol implants; 14 of 29 animals with diethylstilbestrol implants) than animals which did not receive vitamin C supplementation (16 of 23 animals with estradiol implants; 11 of 13 animals with diethystilbestrol implants). Administration of vitamin C to estradiol-treated hamsters for only the first 3 months of the carcinogenesis experiment had no effect on tumor incidence, but vitamin C in drinking water for the last 3 months also lowered incidence. Vitamin C supplementation did not significantly alter the absorption of estrogen from the implant; it did not change the estrogenic effect on the hamsters nor did it significantly influence estrogen-dependent H-301 tumor cell growth. The results were taken as evidence for a mechanism of tumor induction via oxidation of estrogens to reactive metabolites capable of inducing kidney tumors.


Supported by NIH National Cancer Institute Grant CA 27539. Part of this work was published in a preliminary communication (14).

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