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1. Everted sacs of rat duodenum and ileum were used to study the effect of anions and organic ligands on the absorption of zinc. The uptake per unit weight of tissue was greater in duodenum than ileum, and it was influenced by the Zn concentration and pH of the incubation medium.2. The Zn uptake from inorganic salts in simple buffered medium varied in the order zinc sulphate > zinc chloride I, zinc phosphate. Zinc acetate was more effective and zinc citrate less effective than ZnC1,. Addition of aspartic acid or histidine to ZnC1, increased the uptake but galactose or lactose decreased it. 2-Picolinic acid greatly increased the Zn uptake but 4-picolinic acid reduced it.3. When incubated with intestinal sacs after incorporation into a synthetic rat diet, only ZnSO, and 2-picolinic acid increased Zn uptake compared with ZnCI,, but zinc citrate and 4-picolinic acid still tended to decrease it.4. Metabolic balance studies showed no significant differences in the faecal excretion, total excretion or retention of Zn between rats receiving diets containing different forms of Zn. ZnSO,, zinc citrate and particularly 2-picolinic acid increased the urinary excretion of Zn.5. The significance of these results is discussed in relation to the suitability of methods for investigating Zn absorption and the importance of Zn-binding ligands.

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The erythrocyte membrane was investigated in weanling male rats pair fed with magnesium-deficient and control diets for 8 days. Fluorescence polarization studies revealed a 15% increase in the fluidity of membranes from deficient rats. A similar increase in the fluidity of liposomes indicated that protein was not involved. The change was associated with decreased osmotic fragility of intact erythrocytes; the cells lost their biconcavity and had a flattened appearance with surface irregularities. Analysis of the membranes showed decreased amounts of magnesium, cholesterol, and sphingomyelin in the deficient group. The reduced ratios of cholesterol to phospholipid and sphingomyelin to phosphatidylcholine were consistent with the increased fluidity. Addition of physiological amounts of magnesium to the medium rigidified membranes incubated in tris(hydroxymethyl)-aminomethane buffer, and this was prevented by the presence of EDTA. Cross-incubation experiments with erythrocyte ghosts and plasma from the two groups of rats showed that magnesium-deficient plasma increased the fluidity of control ghosts and control plasma rigidified ghosts from magnesium-deficient rats. Addition of sufficient magnesium chloride to raise the magnesium content of deficient plasma to normal had no significant effect. These results show that the increased fluidity of the erythrocyte membrane in magnesium deficiency is due to physicochemical exchange with the plasma. Although magnesium can directly influence membrane fluidity, the change during its deficiency in vivo is mainly mediated indirectly via disturbances in lipid metabolism.