EFFECT OF LEAD ON THE GLYCOSAMINOGLYCANS METABOLISM OF BOVINE AORTIC ENDOTHELIAL-CELLS IN CULTURE

We investigated the effect of lead nitrate (0.1, 1.0, 10 or 20-mu-M) on the metabolism of glycosaminoglycans (GAG) in confluent cultures of bovine aortic endothelial cells. It was found that lead at 10 and 20-mu-M significantly decreased the accumulation of [S-35]sulfate-labeled GAG ([S-35]GAG) both in the cell layer and the medium after a 24-h culture. A time course study showed that 10-mu-M lead decreased the accumulation of [H-3]glucosamine-labeled GAG both in the cell layer and the medium after 24 h and longer. The release of [S-35]GAG from the cell layer during the last 3 h of a 24 h culture was not changed by lead. The detachment of [H-3]thymidine-labeled cells from the monolayer was unaffected by lead. It was shown that lead at 10-mu-M decreased both heparan sulfate and the other GAG in the cell layer; the former was more sensitive to lead treatment. Lead at 20-mu-M and below failed to increase the release of lactate dehydrogenase, suggesting that non-specific cell damage was not caused by lead. From these results, it was suggested that lead decreases endothelial cell heparan sulfate content through a decrease in the GAG production without a non-specific cell damage. Lead may be a risk factor of vascular disorders.