Histochemical study of Hurler's disease by the use of peroxidase-labelled lectins

Abstract

Peroxidase-labelled lectins specific for various carbohydrate residues were used as histochemical reagents in the investigation of Hurler's syndrome. Peanut lectin was used to detect terminal D-galactose, wheatgerm lectin for N-acetyl-D-glucosamine, soybean lectin for N-acetyl-D-galactosamine, Tetragonolobus lotus lectin for alpha-L-fucose and Bandeiraea S. lectin for alpha-D-galactose. It was found that Kupffer cells in the liver and splenic reticulo-endothelial cells contain acid mucopolysaccharides which bind lectins in paraffin sections after appropriate fixation. The pattern of lectin binding suggests that such cells contain significant amounts of D-galactose, L-fucose, N-acetyl-D-galactosamine and N-acetyl-D-glucosamine. It is likely that the last named carbohydrate is present as a polymer. Neurones contain a different carbohydrate, rich in galactose and fucose but poor in N-acetyl-D-glucosamine. This compound is resident to lipid extraction. Hepatocytes, as a rule, do not react with lectins, most likely because of loss of the more soluble mucopolysaccharides during fixation. The results are consistent with the biochemical data of Hurler's syndrome and indicate that lectins can be a useful tool for the investigation of the cytochemistry of storage disorders.

Lectin Histochemistry of Foam Cells in Tissues of Cattle Grazing Brachiaria spp.

“…The lectin staining is also partially comparable to the liver and spleen foamy cells found in human Hurler's disease, positive to PNA, WGA and TPA ( Tetragonolobulus purpureus ) (Faraggiana et al., 1982) and in human sphingomyelinosis, which were stained by PNA, SBA and Con A (Lageron, 1987). However, in cases of feline sphingomyelinosis, the stored material was positive for Con A, RCA‐I and WGA in non‐nervous tissues (Kamiya et al., 1991).…”

“…In the present study, we found that foam cells in liver and lymph node bind PNA, WGA and SBA in a selective way. The staining is particularly clear in liver, probably because hepatocytes, as a rule, do not react with lectins, most probably because of loss of the more soluble glycoconjugates during fixation (Faraggiana et al., 1982). Our results suggest that the foam cells contain large amounts of d ‐galactose, N‐acetyl‐ d ‐galactosamine and N‐acetyl‐ d ‐glucosamine.…”

Avaliação lectino-histoquímica de fígado e linfonodo mesentérico de búfalos mantidos em pastagens de Brachiaria spp.

“…Já a avaliação lectino--histoquímica do fígado e baço de humanos com doença de Niemann-Pick, demonstrou que as lectinas Con-A, PNA e SBA foram as que melhor reagiram com as células afetadas (Lageron 1987) e são semelhantes aos resultados de Gomar et al (2005) e Costa et al (2013). Este padrão lectino-histoquímico também é parcialmente comparável ao encontrado nas células espumosas em fígado e baço de humanos com doença de Hurler (uma mucopolissacaridose tipo I causada pela deficiência da enzima α-L-iduronidase), que são positivas para PNA, WGA e TPA (Tetragonolobulus purpureus) (Faraggiana et al 1982). Todavia, em nenhum dos estudos recém-mencionados testou-se a lectina SWGA nos tecidos avaliados.…”

Quantitative analysis of activated Kupffer cells in viral hepatitis: application of computer image analysis for lectin histochemistry

“…One explanation is that Kupffer cells phagocytosed substances containing carbohydrate residues which bind PNA lectin. In storage disorders such as Hurler's disease and histiocytosis X, both Kupffer cells and macrophages are reported to contain materials positive for PNA lectin (14,15). It is also known that Kupffer cells in acute hepatitis contain digest-PAS positive materials (16).…”