Inhibitory effect of lead on the proliferation of cultured vascular endothelial cells

• Published in: Toxicology (Amsterdam) 1995-01, Vol.95 (1), p.87-92
• Main Authors: Kaji, Toshiyuki, Fujiwara, Yasuyuki, Hoshino, Miho, Yamamoto, Chika, Sakamoto, Michiko, Kozuka, Hiroshi
• Format: Article
• Language: English
• Subjects: Animals; Aorta - cytology; Biological and medical sciences; Cattle; Cell Division - drug effects; Cells, Cultured; Chemical and industrial products toxicology. Toxic occupational diseases; DNA - biosynthesis; DNA synthesis; Endothelial cells; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Fibroblast growth factor; Fibroblast Growth Factor 1 - metabolism; Fibroblast Growth Factor 2 - metabolism; Lead; Lead - pharmacology; Medical sciences; Metals and various inorganic compounds; Nitrates - pharmacology; Proliferation; Thymidine - metabolism; Toxicology
• ISSN: 0300-483X; 1879-3185
• DOI: 10.1016/0300-483X(94)02887-Z

We investigated the effect of lead nitrate (0.5, 1.0, 2.0 or 5.0 μM) on the proliferation of cultured bovine aortic endothelial cells. After exposure to lead, the number of cells and the incorporation of [ 3H]thymidine into the acid-insoluble fraction of the cells were reduced in parallel in a concentration-dependent manner. Histologically, lead treatment resulted in a decrease in the cell number accompanied by a change in the cell shape from polygonal to spindle; however, no degenerative change was observed except in 5.0 μM lead-treated cells. Furthermore, stimulation of [ 3H]thymidine incorporation by either basic or acidic fibroblast growth factor was significantly reduced by lead. However, the leakage of lactate dehydrogenase into the medium from the cells, a marker of nonspecific cell damage, was not changed by lead. From these results, it was revealed that lead inhibits the proliferation of cultured vascular endothelial cells without nonspecific cell damage. Although lead does not destroy the monolayer of endothelial cells, the metal may exhibit its noxious effect in the repair process of the vascular endothelium.