INVITRO EFFECTS OF SELENODIGLUTATHIONE ON CANINE MAMMARY CELLS

Previous studies have shown that seleodiglutathione (SDG) is toxic to canine mammary tumor cell line 13 (CMT-13), reduces the growth of CMT-11, and does not modify the growth of primary non-neoplastic canine mammary (NCM) cells. In the present studies, approximately 6 times more SDG was required to inhibit by 50% the growth of CMT-11 cells compared with CMT-13 cells. Furthermore, these studies reveal that differences in sensitivity among these mammary cells cannot be explained by cellular retention of selenium from SDG. Data obtained using SDG (3.2-mu-M) double labelled with Se-75 and S-35 suggest that differences in the rate of selenium detoxification exist among the three cell cultures examined. The influence of SDG (3.2-mu-M) on intercellular glutathione depended on the cell examined, increasing in CMT-11, decreasing in CMT-13, and unchanged in NCM. Addition of GSH (100-mu-M) partially protected CMT-13 and CMT-11 cells against SDG toxicity. Preincubation of CMT-13 or CMT-11 cells with GSH for 48 hr before the addition of SDG completely prevented the growth inhibition caused by this selencompound. These studies suggest glutathione is critical to the prevention of selenodiglutathione toxicity and accompanying growth depression.