Fujiwara Y, Kaji T, Sakurai S, Sakamoto M, Kozuka H
Department of Environmental Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.
Toxicology. 1997 Feb 28;117(2-3):193-8. doi: 10.1016/s0300-483x(96)03575-5.
We investigated the effect of lead nitrate (0.5-5.0 microM) on the repair of wounded monolayer of cultured bovine aortic endothelial cells. It was morphologically found that lead decreases the appearance of the cells in the wounded area in a concentration-dependent manner without degenerative changes after a 48-h incubation. Although mercury weakly inhibited the repair with nonspecific cell damage, the other cations including bismuth, cobalt, manganese and nickel failed to affect the repair. The inhibition of endothelial repair caused by lead was observed even when stimulated by exogenous either basic or fibroblast growth factor. These results indicated that inhibition of the repair process of damaged endothelial cell layer is a component of lead-induced vascular lesions such as atherosclerosis.
我们研究了硝酸铅（0.5 - 5.0微摩尔）对培养的牛主动脉内皮细胞单层损伤修复的影响。形态学研究发现，在48小时孵育后，铅以浓度依赖的方式减少了损伤区域的细胞出现，且无退行性变化。虽然汞以非特异性细胞损伤的方式微弱地抑制了修复，但包括铋、钴、锰和镍在内的其他阳离子均未影响修复。即使在外源性碱性或成纤维细胞生长因子刺激下，铅对内皮修复的抑制作用依然存在。这些结果表明，受损内皮细胞层修复过程的抑制是铅诱导的血管病变（如动脉粥样硬化）的一个组成部分。
