Lectin binding affinities of induced pancreatic lesions in the hamster model.

We examined the binding pattern of nine lectins to N-nitrosobis(2-oxopropyl)amine (BOP)-induced pancreatic lesions in Syrian hamsters. These lectins were Arachis hypogaea (PNA), Dolichos biflorus (DBA), Griffonia simplicifolia I (GS-I), Helix aspersa (HAA), Helix pomatia (HPA), Sophora japonica (SJA), Ricinus communis I (RCA-I), Triticum vulgaris (WGA) and Ulex europaeus I (UEA-I). All of the lectins reacted in untreated control hamsters to varying intensities with cytoplasmic components of acinar cells. GS-I, HPA, RCA-I and UEA-I bound to the basolateral surface and PNA, HAA and HPA to the luminal surface of these cells. All but GS-I, RCA-I and UEA-I stained the cytoplasm of islet cells diffusely. In untreated control hamsters, some ductal cells bound PNA, HAA and RCA-I, whereas these cells reacted negatively to the remaining six lectins. Ductular cells did not bind any of the nine lectins. Hyperplastic ductal cells in untreated hamsters were reactive with all nine lectins; however the intensity of the reactivity, cellular localization and extent differed for each lectin. In carcinogen-treated hamsters, the binding pattern of the lectins to acinar and islet cells did not differ significantly from that in untreated hamsters, whereas cells of induced ductal and ductular lesions bound each of the lectins in different patterns and intensities. The reaction of UEA-I to induced lesions was most consistent, specific and strong, thereby indicating the presence of L-fucose in glycoproteins produced by altered cells. Although the binding affinity of the lectins to induced hyperplastic lesions differed in both a quantitative and qualitative fashion, all dysplastic and malignant lesions were reactive to each lectin. This result indicates a heterogeneity in the carbohydrate structure of the glycoproteins produced by pancreatic cells during carcinogenicity.