The relative effectiveness of either
sodium selenite or
selenomethionine in the inhibition of mammary
carcinogenesis was studied in virgin female Sprague-Dawley rats. In one experiment, rats were given 50 mg of 1-methyl-1-nitrosourea per kg of
body weight s.c. at 50 days of age. Beginning 7 days post-1-methyl-1-nitrosourea, they were assigned to a basal diet containing 0.1 ppm of
selenium or basal diet supplemented to contain either 4, 5, or 6 ppm of
selenium as
sodium selenite or 5 or 6 ppm of
selenium as
selenomethionine.
Selenium treatment was continued until termination of the study 135 days after 1-methyl-1-nitrosourea treatment.
Sodium selenite, at the 5-ppm level, was the most effective chemopreventive agent. The highest level of
selenomethionine (6 ppm) caused grossly apparent liver damage. No liver damage was noted in
sodium selenite-treated rats. In a second experiment, rats were given 5 mg of
7,12-dimethylbenz(a)anthracene at 50 days of age. Beginning 7 days after
7,12-dimethylbenz(a)anthracene treatment, rats were assigned randomly to the control group or to one of two
selenium treatment groups receiving either 3.4 ppm of
selenium as
sodium selenite or 3.4 ppm as
selenomethionine in their
drinking water.
Selenium supplementation was continued throughout the study until its termination at 111 days postcarcinogen .
Sodium selenite significantly reduced
cancer incidence and the average number of
cancers per rat. Treatment with
selenomethionine was less effective and caused severe liver damage. Although both
sodium selenite and
selenomethionine can inhibit some aspect of the postinitiation stage(s) of mammary
carcinogenesis,
selenium provided as
sodium selenite was the more effective and less toxic of the two chemicals. Increasing the dose of
sodium selenite above 5 ppm did not enhance the inhibitory activity of
selenium.