Kaji T, Fujiwara Y, Hoshino M, Yamamoto C, Sakamoto M, Kozuka H
Department of Environmental Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.
Toxicology. 1995 Jan 6;95(1-3):87-92. doi: 10.1016/0300-483x(94)02887-z.
We investigated the effect of lead nitrate (0.5, 1.0, 2.0 or 5.0 microM) 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 microM 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.
我们研究了硝酸铅（0.5、1.0、2.0或5.0微摩尔）对培养的牛主动脉内皮细胞增殖的影响。暴露于铅后，细胞数量以及[3H]胸腺嘧啶核苷掺入细胞酸不溶性部分的量呈浓度依赖性平行减少。组织学上，铅处理导致细胞数量减少，同时细胞形状从多边形变为纺锤形；然而，除了5.0微摩尔铅处理的细胞外，未观察到退行性变化。此外，碱性或酸性成纤维细胞生长因子对[3H]胸腺嘧啶核苷掺入的刺激作用被铅显著降低。然而，作为非特异性细胞损伤标志物的乳酸脱氢酶从细胞泄漏到培养基中的情况未因铅而改变。从这些结果可以看出，铅抑制培养的血管内皮细胞增殖而无特异性细胞损伤。虽然铅不会破坏内皮细胞单层，但这种金属可能在血管内皮的修复过程中表现出有害作用。
