Zinc: Health Effects and Research Priorities for the 1990s

Abstract

This review critically summarizes the literature on the spectrum of health effects of zinc status, ranging from symptoms of zinc deficiency to excess exposure. Studies on zinc intake are reviewed in relation to optimum requirements as a function of age and sex. Current knowledge on the biochemical properties of zinc which are critical to the essential role of this metal in biological systems is summarized. Dietary and physiological factors influencing the bioavailability and utilization of zinc are considered with special attention to interactions with iron and copper status. The effects of zinc deficiency and toxicity are reviewed with respect to specific organs, immunological and reproductive function, and genotoxicity and carcinogenicity. Finally, key questions are identified where research is needed, such as the risks to human health of altered environmental distribution of zinc, assessment of zinc status in humans, effects of zinc status in relation to other essential metals on immune function, reproduction, neurological function, and the cardiovascular system, and mechanistic studies to further elucidate the biological effects of zinc at the molecular level. - There is considerable evidence that zinc deficiency in humans is a serious worldwide problem and outweighs the potential problem of accidental, self-imposed, or environmental exposure to zinc excess. Acute deficiency (1) and chronic deficiency (2) are well-known entities in human populations and are probably much more common than generally recognized. The importance of zinc for human health was first documented in 1963 (3) Telephone (617) (617) 638-4329. E-mail: ctwalsh~bu.edu renal disease, and other chronically debilitating diseases are now known to be predisposing factors for zinc deficiency in humans (4).Zinc deficiency is reflected in clinical syndromes which affect men and women of all ages and all socioeconomic and cultural classes in the United States. It is neither prevalent in any specific area of the United States nor associated with any specific or definitive biochemical marker, which can make its identification difficult and confusing. Its presence is manifested by a wide spectrum of symptoms, from acute, life threatening problems to mild subclinical or marginal disorders which may only vaguely disturb well being. The acute problems are often seen in profoundly ill patients treated in hospitals, whereas subclinical problems may be so vague that patients seek assistance outside traditional medical practice.Based upon clinical data and using traditional, epidemiologic techniques, Henkin and Aamodt (5) have reclassified zinc deficiency into three syndromes; these are a) acute, b) chronic, and c) subacute zinc deficiency. Acute zinc deficiency is relatively uncommon and follows parenteral hyperalimentation or oral L-histidine administration. Chronic zinc deficiency is more common, usually resulting from chronic dietary lack of zinc. Subacute or latent zinc deficiency is the most common of these syndromes. It is estimated that there are 4...

Regulation of the PIS1-encoded Phosphatidylinositol Synthase in Saccharomyces cerevisiae by Zinc

“…transcription factors, chaperones, lipid-binding proteins) (36,37). Zinc deficiency in rats is associated with oxidative damage to DNA, lipids, and proteins (38), and in humans, it is manifested by defects in appetite, cognitive function, embryonic development, epithelial integrity, and immune function (39). Despite its essential nature, zinc is toxic to cells when accumulated in excess amounts (35).…”

Zeolites versus Lead Toxicity

“…Copper distribution has been estimated in human tissues [64], and transport mechanisms and serum levels of copper have been well studied [65]. The main storage sites of cadmium are liver and kidney [11,[66][67][68][69].…”

Low intracellular zinc induces oxidative DNA damage, disrupts p53, NFκB, and AP1 DNA binding, and affects DNA repair in a rat glioma cell line

“…Zinc is a component of Ͼ1,000 proteins including DNAbinding proteins with zinc fingers, copper͞zinc superoxide dismutase (CuZnSOD), and several proteins involved in DNAdamage repair such as p53, which is mutated in half of human tumors (8). It can be hypothesized that insufficient zinc intake can impair antioxidant defenses and compromise DNA-repair mechanisms, making the cell highly susceptible to oxidative DNA damage.…”