Cells of the Raji human [Burkitts'' lymphoma] lymphoblastoid line, when pretreated with the metabolic inhibitor puromycin, were susceptible to killing by the isolated proteins of the complement (C) attack mechanism (C5-9[the 5th C component through C9]). Incubation of 51Cr-labeled lymphoblastoid cells with purified .**GRAPHIC**. and C7 resulted in the formation of a lymphoblast- .**GRAPHIC**. intermediate, and the addition of purified human C8 and C9 resulted in release of 51Cr from these cells. Serum .**GRAPHIC**. inhibitors .**GRAPHIC**. purified human lipoproteins and dextran sulfate, each previously shown to inhibit the attachment of the .**GRAPHIC**. trimolecular complex to erythrocytes, also inhibited the formation of .**GRAPHIC**. and as a consequence, .**GRAPHIC**. cytotoxicity; the polycation protamine sulfate counteracted the inhibitory effect of dextran sulfate. The potential for damage of bystander nucleated cells exists when .**GRAPHIC**. is generated in solution, and is influenced by agents known to modulate the hemolytic activity of .**GRAPHIC**. These mechanisms may be involved in the control of the function and the viability of various nucleated cells.