Four different canine mammary
tumor (CMT) cell lines and a nonneoplastic primary culture of mammary cells were examined for their in vitro responsiveness to
selenium supplementation. These cell lines were found to vary in their metabolic response to increasing concentrations of
selenium. Sensitivity to
selenium, as
sodium selenite, increased with increasing concentrations of this
trace element in all of the neoplastic lines. These data also suggest that increasing the plating density of
tumor cells further increases the sensitivity to
selenium. A relatively
selenium-sensitive cell line (CMT-13) and relatively insensitive cell line (CMT-11) were characterized on the basis of reduced growth resulting from
selenium supplementation. Increasing the concentration of
selenium to 0.75 microgram/ml depressed the growth of CMT-13 and CMT-11 cells by 75% and 11%, respectively, while no inhibition was observed in nonneoplastic cells. These cell lines also varied in their sensitivity to different forms of
selenium.
Selenodiglutathione was the most effective form of
selenium examined that inhibited
tumor cell growth. The sensitivity of the neoplastic lines was
selenodiglutathione much greater than
sodium selenite much greater than
selenocystine greater than
selenomethionine. None of the forms of
selenium examined inhibited the growth of the nonneoplastic mammary cells in culture. Supplementation with
sodium selenite (1 microgram Se per ml) for 60 min resulted in a dramatic depression in
RNA biosynthesis in CMT-13, but not CMT-11 or nonneoplastic cells.