The effect of treatment of target tumor cells with glutaraldehyde (GA) on antibody-dependent macrophage-mediated cytolysis was investigated in a C3H/He mouse-MM46 syngeneic tumor system. GA-treated tumor cells were more susceptible to antibody-dependent macrophage-mediated cytolysis. Lysis of GA-treated cells was observed with less antibody and fewer macrophages than that of untreated cells. However, GA-treated cells had the same amount of antigen sites and the same activity of antibody-dependent attachment to macrophages as do fresh tumor cells. Thus, this enhancement of lysis did not occur at the antibody-binding step or the early step of contact between macrophages and tumor cells but at the subsequent step, perhaps at the tumor lysis step. GA-treated tumor cells could not synthesize DNA or RNA, but cells attenuated with mitomycin C or actinomycin D were not susceptible to antibody-dependent macrophage-mediated cytolysis. These results suggest that the cytostatic effect of GA does not involve change in susceptibility of target cells to lysis, but some impairment of the cell membrane. GA-treated tumor cells could not grow in vivo and could induce antitumor immunity.
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