Iwata-Dohi N, Esumi-Kurisu M, Ikenami M, Sadatsune K, Mizuno D, Yamazaki M
Cancer Res. 1982 Aug;42(8):3196-200.
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.
在C3H/He小鼠-MM46同基因肿瘤系统中,研究了用戊二醛(GA)处理靶肿瘤细胞对抗体依赖性巨噬细胞介导的细胞溶解作用的影响。经GA处理的肿瘤细胞对抗体依赖性巨噬细胞介导的细胞溶解更敏感。与未处理的细胞相比,观察到经GA处理的细胞在抗体和巨噬细胞数量较少的情况下发生溶解。然而,经GA处理的细胞具有与新鲜肿瘤细胞相同数量的抗原位点以及相同的抗体依赖性与巨噬细胞结合的活性。因此,这种溶解增强并非发生在抗体结合步骤或巨噬细胞与肿瘤细胞接触的早期步骤,而是发生在随后的步骤,可能是在肿瘤溶解步骤。经GA处理的肿瘤细胞无法合成DNA或RNA,但用丝裂霉素C或放线菌素D处理减弱的细胞对抗体依赖性巨噬细胞介导的细胞溶解不敏感。这些结果表明,GA的细胞抑制作用并不涉及靶细胞对溶解敏感性的改变,而是细胞膜的某些损伤。经GA处理的肿瘤细胞在体内无法生长,并可诱导抗肿瘤免疫。