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Effect of Zinc Deficiency and Food Restriction in Rats on Erythrocyte Membrane Zinc, Phospholipid and Protein Content^1,2,

Department of Biochemistry, University of Missouri, Columbia, MO 65211

Zinc deficiency in rats increases the osmotic fragility of erythrocytes, suggesting a structural defect in the plasma membrane. The purpose of this study was to determine the effect of zinc deficiency on membrane components that might be responsible for the increased fragility. Immature male rats were fed for 3 wk a zinc-deficient (0.5 mg Zn/kg) or a control (100 mg Zn/kg) diet either ad libitum or pair-fed. Red blood cell membranes were analyzed for zinc after wet ashing in nitric-perchloric acid. The fatty acid composition of membrane phosphatidylcholine and phosphatidylethanolamine was determined by gas-liquid chromatography, and the protein composition was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The membrane zinc concentration was decreased by zinc deficiency, but returned to control levels upon repletion with a zinc-adequate diet for 3 d. The increased osmotic fragility was also restored to the control level during the same repletion period, suggesting that zinc is an important determinant of membrane stability. The phospholipid fatty acid composition was altered by zinc deficiency, but these changes were not rapidly reversed by repletion. The membrane cholesterol:phospholipid ratio was also increased by zinc deficiency. Zinc status had no influence on the membrane protein profiles of the components visualized by staining. Only the concentration of membrane zinc correlated with osmotic fragility during zinc depletion and repletion.

KEY WORDS: • zinc deficiency • male rats • osmotic fragility • erythrocyte membrane zinc • membrane phospholipids • energy restriction

¹ Supported in part by National Institutes of Health Grants HL 11614 and NS 25395. U.S. Department of Health and Human Services.

² Contribution of the Missouri Agricultural Experiment Station, Journal Series No. 10754

³ To whom correspondence should be addressed.

Manuscript received 10 February 1989. Revision accepted 5 June 1989.

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