Proteoglycans in the compressed region of human tibialis posterior tendon and in ligaments.

Proteoglycan content and tissue morphology were examined in tendons and ligaments from 24 cadavers, ranging in age at the time of death from 1.5 months to 83 years. The region of the human tibialis posterior tendon that passes under the medial malleolus was characterized by cells having a rounded shape, positive staining with alcian blue, and higher glycosaminoglycanuronic acid content than in the more proximal region of the same tendon. Analysis of proteoglycans by sodium dodecyl sulfate/polyacrylamide gel electrophoresis indicated that the predominant small proteoglycan of the proximal/tensional region was decorin, whereas two types of small proteoglycans (decorin and biglycan) and large proteoglycans were present in the region passing under the medial malleolus and presumably subjected to compressive and shear forces in addition to tension. The pattern of proteoglycan accumulation in the compressed region of tendon was basically similar for all individuals and showed no distinctive trends related to age after puberty. In terms of type and amount of proteoglycan, the patellar tendon was like the tensional region of the tibialis posterior. Glycosaminoglycan content in the lateral collateral ligament and anterior cruciate ligament, however, was twofold higher than in the tendons. The ligaments contained large as well as small proteoglycans, just as in the compressed region of tendon.

Liver damaging effect of suramin in normal and carbon-tetrachloride treated rats.

Male Fischer 344 (F344) rats were treated with phenobarbital + carbon tetrachloride (CCl4) for 16 weeks to induce liver cirrhosis. Another group of rats received 50 mg/kg iv suramin once a week for 16 weeks. The third group of rats was treated with both phenobarbital + CCl4 and suramin. After 16 weeks of suramin treatment, a massive periportal infiltration composed of macrophages, many of them containing glycosaminoglycans in their cytoplasm, mast cells, and other inflammatory cells were observed. This lesion was added to the liver cirrhosis caused by CCl4 in the group treated with suramin and CCl4. The changes in glycosaminoglycan metabolism caused by suramin did not influence the CCl4 cirrhosis. Since suramin has been reported to be a prototype of a new generation of antitumor compounds, we suggest caution in the use of chronic suramin treatment, especially in patients with livers which are already damaged.