The objectives of this study were (1) to quantify galaptin, an endogenous lectin, and galaptin-binding glycoconjugates present in normal serum, (2) to determine if these components were altered in the serum and effusions of carcinoma patients with advanced disease, and (3) to determine if ovarian carcinoma cells synthesize and release soluble galaptin inhibitors. Serum from healthy females (n = 10) had a mean galaptin content of 96 ± 40 ng/ml. Galaptin levels in carcinoma patient serum (n = 29) were depressed (mean 21 ± 23 ng/ml; p < 0.0001). Galaptin was not detected in 6 of 8 ovarian carcinoma patient sera. Effusions (n = 17) had a mean galaptin content of 358 ± 326 ng/ml. Assays involving inhibition of binding of galaptin-peroxidase conjugates to asialofetuin were carried out to evaluate the levels of galaptin-binding glycoconjugates in serum and effusions. The mean inhibition titer of normal serum (n = 12) was 75 ± 38. Patient serum (n = 28) had an elevated inhibitor content (mean titer = 304 ± 155; p < 0.0001). Effusions (n = 17) also had a higher inhibitor content relative to normal serum (mean titer = 247 ± 202; p = 0.0037). Ovarian carcinoma cells isolated from effusions and cultured in vitro were shown to synthesize and release into the medium galaptin-binding glycoconjugates of molecular mass 100-200 kD. An ovarian carcinoma cell line, A121, released galaptin-binding glycoconjugates of molecular mass ≥ 200 kD into the medium. The data presented show that the levels of soluble galaptin and galaptin-binding glycoconjugates in the serum of advanced cancer patients are perturbed relative to normal femal