In order to examine the ability of complement to solubilize immune complexes (IC) in vivo, acute or chronic serum sickness nephritis was induced in 10 rabbits and 11 rats with by injection of BSA as an antigen (Ag). The animals were divided into two groups. The first received 500U or 50U/week cobra venom factor (CVF) administered intraperitoneally to reduce serum complement levels and complement-mediated solubilization of immune complexes. On the other hand, the second group received 2ml or 0.2ml/week turpentine oil (TO) injected interamuscularly to elevate serum complement levels and complement-mediated solubilization of immune complex. Renal biopsies were performed weekly with each animal, and these specimens were stained for antigen (BSA), antibody (IgG) and complement (C3) by immunofluorescence techniques. Results showed a significant difference between TO-, and CVF-treated animals with respect to the decline of IC in kidney lesions. No detectable IC (especially BSA) remained in the renal glomeruli of TO-treated nephritic animals, indicating that complement might act in vivo to solubilize IC deposited in tissues.