Hennig B, Wang Y, Ramasamy S, McClain C J
Department of Nutrition and Food Science, University of Kentucky, Lexington.
J Nutr. 1992 Jun;122(6):1242-7. doi: 10.1093/jn/122.6.1242.
Zinc is necessary for normal membrane function and stability. We postulated that Zn deficiency may disrupt the integrity of the vascular endothelium by decreasing its barrier function. To test this hypothesis, endothelial cells were cultured on polycarbonate filters and exposed to media enriched with either 1% fetal bovine serum (FBS) (low FBS; total Zn, 1.07 mumols/L medium) or 5% FBS (control; total Zn, 2.29 mumols/L) or low FBS plus two supplemental levels of Zn, 3.36 and 5.66 mumols total zinc/L. Endothelial cell barrier function, expressed as albumin transfer across cultured endothelial monolayers, was significantly lower in cultures exposed to low FBS compared with control medium. Supplementation with 5.66 mumols total Zn/L completely restored endothelial barrier function. A divalent cation chelator, 1,10-orthophenanthroline, was used to induce Zn deficiency in vitro. Compared with control cultures, the presence of 1,10-orthophenanthroline in the culture medium resulted in markedly lower endothelial barrier function that was increased by the addition of Zn but not calcium or magnesium. Activity of the membrane-bound zinc-dependent angiotensin-converting enzyme (ACE) was depressed by low zinc medium, whereas membrane-bound Ca(2+)-ATPase and total ATPase were not depressed. Furthermore, cells cultivated in low zinc medium did not have greater cytosolic release of adenine, indicating no increase in cell injury or death. These data suggest that Zn is vital to endothelial cell integrity and that Zn may play an important role in vascular endothelial barrier function.
锌对于正常的膜功能和稳定性是必需的。我们推测锌缺乏可能通过降低血管内皮的屏障功能而破坏其完整性。为了验证这一假设，将内皮细胞培养在聚碳酸酯滤膜上，并使其暴露于富含1%胎牛血清（FBS）（低FBS；总锌含量为1.07μmol/L培养基）或5% FBS（对照；总锌含量为2.29μmol/L）或低FBS加两种补充水平锌（总锌含量分别为3.36和5.66μmol/L）的培养基中。以内皮细胞单层中白蛋白转运来表示的内皮细胞屏障功能，在暴露于低FBS的培养物中显著低于对照培养基。补充5.66μmol/L总锌可完全恢复内皮屏障功能。一种二价阳离子螯合剂1,10-邻菲罗啉用于在体外诱导锌缺乏。与对照培养物相比，培养基中存在1,10-邻菲罗啉导致内皮屏障功能显著降低，添加锌可使其增加，但添加钙或镁则不能。膜结合的锌依赖性血管紧张素转换酶（ACE）的活性被低锌培养基抑制，而膜结合的Ca(2+)-ATP酶和总ATP酶未被抑制。此外，在低锌培养基中培养的细胞没有更高的腺嘌呤胞质释放，表明细胞损伤或死亡没有增加。这些数据表明锌对于内皮细胞完整性至关重要，并且锌可能在血管内皮屏障功能中起重要作用。
