Zinc deficiency increases the osmotic fragility of rat erythrocytes.

Zinc deficiency in rats causes increased osmotic fragility of their erythrocytes. This study was designed to determine the relationship of food intake and dietary sulfur amino acid level to the effect of low zinc status on fragility. Immature rats were fed for a 3-wk period a low zinc diet (less than 1 mg/kg) based on isolated soybean protein or a similar control diet (100 mg Zn/kg diet) supplied either ad libitum or by pair feeding. Fragility was measured by the degree of hemolysis in hypotonic saline solutions. In the first experiment, zinc deficiency resulted in higher fragility than in ad libitum controls; pair-fed controls were intermediate and not different from either. Experiment 2 included two levels of methionine, 0.4 and 0.9%, and two of zinc, 0 and 100 mg Zn/kg diet. At the 0.4%, but not at the 0.9% methionine level, hemolysis of red blood cells from the zinc-deficient rats was significantly greater than those from either pair-fed or ad libitum controls. Repletion for 1 or 2 d completely alleviated the increased fragility, but in vitro addition of zinc had no effect. Restricted intake of the zinc-adequate diet reversed the fragility within 1 d as readily as did ad libitum intake. Thus, the osmotic fragility induced by zinc deficiency was prevented by high sulfur amino acid intake and was readily reversed by dietary zinc. It is postulated that extracellular or membrane-bound zinc protects a component of the membrane that is essential to its function, and that reversal of the defect requires an in vivo metabolic process.