Zinc metabolism in infection.

1. Multiple sequential changes in zinc metabolism occur during infectious illnesses. These are characterized by early redistribution and by the late occurrence of direct zinc losses. Redistribution is accompanied in many infections by a decline in plasma concentrations before or with onset of illness. Although late losses of zinc have not been confirmed by metabolic balances during infection, losses may be inferred because: a) they accompany the catabolic phase of other illnesses, b) urinary losses have been observed during infections in which they were measured, and c) infections may exaggerate losses via sweat or diarrhea. 2. Leukocytic endogenous mediator (LEM), appears to stimulate the initial changes in zinc redistribution. Although LEM has not been isolated in pure form, it can now be separated by physiocochemical means from endogenous pyrogen and other mediator substances released by activated phagocytic cells. 3. Early zinc redistribution may be a purposeful physiological event which serves as a host defense mechanism. Redistribution may influence the stability of cellular membranes, augment the functional ability of phagocytic cells and certain classes of lymphocytes, aid in the synthesis of nucleic acids and proteins, and contribute to the production of various zinc metalloenzymes. 4. Zinc therapy has not been shown experimentally to produce a beneficial effect in any infectious disease studied in animal models.