Rifkin M R
J Cell Biochem. 1983;23(1-4):57-70. doi: 10.1002/jcb.240230107.
The specific lysis of bloodstream trypanosomes by serum from a nonpermissive mammalian host is the result of interaction between the serum trypanocidal factor (high-density lipoprotein) and the trypanosome surface. The studies described in this paper attempt to define further the mode of action of this cytotoxic lipoprotein. The binding of high-density lipoprotein to Trypanosoma brucei was instantaneous at 4 degrees C and readily reversible. Binding was not mediated by the surface glycoprotein as removal of the surface coat enhanced binding at 4 degrees C, and no stable glycoprotein-lipoprotein complex could be detected. Pretreatment of trypanosomes with the cross linker dimethylsuberimidate rendered cells resistant to lysis. Addition of membrane-stabilizing drugs, such as cytochalasins C, D, and E, and local anesthetics (dibucaine, tetracaine, and procaine), also inhibited high-density lipoprotein-induced cell lysis. The data presented support the idea that at 37 degrees C lateral diffusion of the variant surface glycoprotein, an integral membrane protein, allows maximal high-density lipoprotein-cell interaction in serum-sensitive cells, and that altered properties of the plasma membrane induced by low temperature or the addition of cytochalasins, local anesthetics, or zinc inhibit this interaction, possibly by increasing the shielding of the plasma membrane by more rigidly anchored surface glycoprotein molecules.
非容许性哺乳动物宿主血清对血流中锥虫的特异性裂解是血清杀锥虫因子（高密度脂蛋白）与锥虫表面相互作用的结果。本文所述研究试图进一步明确这种细胞毒性脂蛋白的作用方式。高密度脂蛋白与布氏锥虫在4℃时的结合是瞬时的且易于逆转。这种结合不是由表面糖蛋白介导的，因为去除表面被膜会增强在4℃时的结合，并且未检测到稳定的糖蛋白 - 脂蛋白复合物。用交联剂亚胺酯预处理锥虫可使细胞抵抗裂解。添加膜稳定剂药物，如细胞松弛素C、D和E以及局部麻醉剂（丁卡因、丁哌卡因和普鲁卡因），也能抑制高密度脂蛋白诱导的细胞裂解。所呈现的数据支持这样的观点，即在37℃时，作为整合膜蛋白的可变表面糖蛋白的侧向扩散使血清敏感细胞中的高密度脂蛋白与细胞的相互作用达到最大，并且低温或添加细胞松弛素、局部麻醉剂或锌所诱导的质膜性质改变会抑制这种相互作用，可能是通过增加更牢固锚定的表面糖蛋白分子对质膜的屏蔽作用来实现的。
