Oteiza P I, Cuellar S, Lönnerdal B, Hurley L S, Keen C L
Department of Nutrition, University of California, Davis 95616.
Teratology. 1990 Jan;41(1):97-104. doi: 10.1002/tera.1420410110.
The hypothesis that one of the biochemical lesions underlying zinc deficiency-induced teratogenicity is altered microtubule formation was tested. Day 19 fetuses from zinc-deficient Sprague-Dawley dams were characterized by low brain supernate zinc concentrations and slow brain tubulin polymerization rates compared to controls. Brain supernate tubulin and protein concentrations were similar in zinc-deficient and control fetuses. In vitro brain tubulin polymerization rates were increased following addition of zinc to either control or zinc-deficient brain supernates; however, the stimulatory effect of added zinc on polymerization was significantly higher in brain supernates obtained from zinc-deficient fetuses compared to controls. These results support the idea that one effect of fetal zinc deficiency is a reduction in tubulin polymerization, which in turn may result in altered microtubule function.
对锌缺乏诱导致畸性的潜在生化损伤之一是微管形成改变这一假说进行了检验。与对照组相比，缺锌的斯普拉格-道利母鼠所产第19天胎儿的特点是脑上清液锌浓度低，脑微管蛋白聚合速率慢。缺锌胎儿与对照胎儿的脑上清液微管蛋白和蛋白质浓度相似。向对照或缺锌的脑上清液中添加锌后，体外脑微管蛋白聚合速率均增加；然而，与对照组相比，从缺锌胎儿获得的脑上清液中添加锌对聚合的刺激作用明显更高。这些结果支持这样一种观点，即胎儿缺锌的一个影响是微管蛋白聚合减少，这反过来可能导致微管功能改变。
