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Zinc Deficiency Alters Barrier Function of Cultured Porcine Endothelial Cells¹

Bernhard Hennig^*,, Yin Wang^*,, Santhini Ramasamy^* and Craig J. McClain^,

^* Department of Nutrition and Food Science Graduate Center for Toxicology Department of Medicine, University of Kentucky and Lexington VA Medical Center, Lexington, KY 40506

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 µmol/L medium) or 5% FBS (control; total Zn, 2.29 µmol/L) or low FBS plus two supplemental levels of Zn, 3.36 and 5.66 µmol 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 µmol 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 Ca²⁺-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.

KEY WORDS: • zinc • zinc deficiency • endothelium • membranes • angiotensin converting enzyme • porcine cells

¹ Supported in part by grant HL-36552 from the National Heart, Lung, and Blood Institute, National Institutes of Health Grant 1 R01 NS22712-01A1; grants from the National Live Stock and Meat Board and the Kentucky Beef Cattle Association; Department of Education #G-008720136; the Kentucky Agricultural Experiment Station (article number 90-9-203), CRC grant #MO1RRO26O2-O7, and the Veterans Administration.

Manuscript received 1 April 1991. Revision accepted 23 January 1992.

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