Date of Award:

5-1971

Document Type:

Thesis

Degree Name:

Master of Science (MS)

Department:

Nutrition, Dietetics, and Food Sciences

Department name when degree awarded

Nutrition and Food Sciences

Committee Chair(s)

Ethelwyn B. Wilcox

Committee

Ethelwyn B. Wilcox

Committee

Deloy G. Hendricks

Committee

Arthur Mahoney

Abstract

Three experiments were conducted to study the effect of zinc deficiency on hemoglobin, red cell counts, red cell fragility, storage of erythropoietic minerals in livers and circulating levels of zinc, iron and copper in the rat.

In the experiment 1, twenty weanling rats were divided into four groups. Two groups were fed zinc-deficient diet ( <0.5 ppm); and two groups, zinc-supplemented diet (50 ppm). The rats in the first and third groups were bled three times a week (bled), however the rats in remaining groups were bled once a week (non-bled). All rats received ad libitum food.

Mean food intake per day was considerably less for zinc-deficient rats than that for zinc-supplemented rats. Approximately 2 to 3 times as much food was required for each gram of body weight gained by the zinc-deficient group as by the controls.

In the experiment 2, fifty-two male weanling rats were divided into six groups; three groups were bled and three non-bled. The 2nd and 5th groups of (zinc-supplemented) rats were pair-fed with the same amount of food as the 1st and 4th zinc-deficient groups ate. The 3rd and 6th groups (control) were fed ad libitum.

Hemoglobin levels were lower (P < 0.05) in bled groups than in the non-bled groups irrespective of zinc treatment in experiment 1 and 2. Within the bled and non-bled groups the zinc-deficient rats consistently exhibited decreased hemoglobin values as compared to zinc-supplemented rats. All zinc-deficient rats had a significantly lower (P < 0.05) liver zinc content than did the zinc-supplemented ones. There was no difference in iron as well as in copper content of the livers among the groups of experiment 1. However, in experiment 2, copper content per liver was significantly less (P < 0.05) in zinc-deficient rats than in the zinc-supplemented rats. Serum zinc values were lower in zinc deficient than in control rats. No differences in the concentration of copper in the serum were observed.

Red-blood-cell membrane fragility in experiment 2 indicated that there were no differences in percent hemolysis among bled groups. However, percent hemolysis was significantly lower (P < 0.05) in zinc-deficient non-bled groups which clearly indicated that treatment did affect hemolysis. Among other possibilities this might be attributed to more rapid turn-over of red-blood-cells in zinc-deficient rats.

In the experiment 3, twenty-four male weanling rats were divided into three groups; one group of zinc-supplemented rats was pair-fed to the zinc-deficient group; and remaining control group, fed ad libitum. All the rats were bled once a week. After 28 days of feeding the rats were injected with 2-C14-glycine (5 μc/100 g body weight). It was observed that incorporation of glycine into hemoglobin in the zinc deficient rats was significantly (P < 0.05) more than in the zinc-supplemented rats. With the limited data it is difficult to draw a definite conclusion. Perhaps, it may be true that the red-blood-cells of zinc-deficient rats might have a short life span resulting in the new red cell formation.

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