Distribution of protein-bound zinc in normal and cirrhotic serum

Abstract

The distribution of 65Zn among the serum proteins of 18 cirrhotic patients and 10 normal individuals was studied. Total zinc was measured in each serum. Zinc was bound to albumin, transferrin and α2-macroglobulin in all subjects. It was bound to IgG in all cirrhotics and five of ten normals. Utilizing the percentage distribution of 65Zn and total serum zinc, the amount bound in each fraction was calculated. Albumin-bound zinc correlated well with total serum zinc (r = 0.97). Total serum zinc was lower in cirrhotics than in normals (p < 0.01). The low serum zinc found in cirrhotics appears to be a function of serum albumin concentration. Zinc was consistently bound to transferrin and α2-macroglobulin. The total amount bound to these proteins (Tf-α2M) was of remarkably constant and equivalent size in normals and cirrhotics. Transferrin concentration was significantly lower (p < 0.01) in cirrhotics. The mean concentration of α2-macroglobulin was higher in cirrhotics although the difference was not significant (p < 0.10). There appears to be a reciprocal relationship between the amount of zinc bound to transferrin and that bound to α2-macroglobulin. However, the total amount bound to Tf-α2M remains remarkably constant even when total serum zinc falls as low as 12 μg./ml. The constancy of the amount of zinc bound to Tf-α2M implies metabolic control of this fraction. When serum zinc falls to very low levels, it may account for nearly one-half of the total serum zinc. It is suggested that transferrin and α2-macroglobulin may have an important role in internal zinc exchange. The distribution of 65Zn among the serum proteins of 18 cirrhotic patients and 10 normal individuals was studied. Total zinc was measured in each serum. Zinc was bound to albumin, transferrin and α2-macroglobulin in all subjects. It was bound to IgG in all cirrhotics and five of ten normals. Utilizing the percentage distribution of 65Zn and total serum zinc, the amount bound in each fraction was calculated. Albumin-bound zinc correlated well with total serum zinc (r = 0.97). Total serum zinc was lower in cirrhotics than in normals (p < 0.01). The low serum zinc found in cirrhotics appears to be a function of serum albumin concentration. Zinc was consistently bound to transferrin and α2-macroglobulin. The total amount bound to these proteins (Tf-α2M) was of remarkably constant and equivalent size in normals and cirrhotics. Transferrin concentration was significantly lower (p < 0.01) in cirrhotics. The mean concentration of α2-macroglobulin was higher in cirrhotics although the difference was not significant (p < 0.10). There appears to be a reciprocal relationship between the amount of zinc bound to transferrin and that bound to α2-macroglobulin. However, the total amount bound to Tf-α2M remains remarkably constant even when total serum zinc falls as low as 12 μg./ml. The constancy of the amount of zinc bound to Tf-α2M implies metabolic control of this fraction. When serum zinc falls to very low levels, it may account for nearly one-half of the total serum zinc. It is suggested that transferrin and α2-macroglobulin may have an important role in internal zinc exchange.