The effects of gold sodium thiomalate (GST) on murine spleen cells were investigated using in vitro mitogen blastogenesis techniques. Addition of GST to intact spleen cells resulted in a decreased blastogenic response to the T cell mitogen, concanavalin A (Con A). Thymidine uptake of spleen cells depleted of macrophages and cultured with Con A and GST demonstrated biphasic effects. At 2.5 pg Con A/ml, blastogenesis of macrophage depleted spleen cells was inhibited to a lesser degree than intact spleen cells; whereas, at 0.5 pg Con A/ml, the macrophage depleted spleen cells were inhibited to a greater degree than the intact spleen cells. Addition of GST at intervals ranging from 0 to 48 hours indicated that inhibition occurred within 36 hours following mitogen stimulation. These results suggest that GST inhibits early events of lymphocyte activation by direct interaction with lymphocytes.

Balb/c normal mice were used to study the effects of gold sodium thiomalate (GST) on intact, nonadherent, and adherent mononuclear spleen cells. The three populations were tested for the following aspects: in vitro effects of GST on the mitogen-triggered DNA synthesis; intracellular levels of cyclic AMP; and chemotaxis ability. These studies showed that GST inhibited the proliferative responses of all three populations as the concentration of GST increased. Cyclic AMP levels in the nonadherent population increased as the GST concentration increased. GST had a biphasic effect on the adherent population. At concentrations of 5 and 10 jag/ml, GST suppressed the cyclic AMP levels, and at concentration of 50 pg/ml it enhanced the cyclic AMP levels. GST had no effect on the cyclic AMP levels in the intact mononuclear spleen cells. GST appeared to have an inhibitory effect on the chemotaxis ability of all three populations of spleen cells.