Interactions of Some Trace Element Nutrients and Xenobiotics Metabolism

Abstract

Requirements by animals and humans for dietary trace nutrients are often modified by interactions with other nutrients, with nonnutritive food components, with food additives and drugs, with environmental contaminants such as agricultural or industrial chemicals, and with natural xenobiotics such as mold toxins and toxicants in plants. Some selected examples of these interactions are reviewed briefly to illustrate various types of nutrient x xenobiotics interactions. For example, Zn requirements are increased by excessive dietary Ca, Cu or Fe, by dietary phytate, oxalate or (soluble) silicate, by Cd or Ga, by certain types of dietary fiber, and by ingestion of some kinds of clay. Certain types of mycotoxicoses (e.g., sporedesmin) and toxicoses caused by plant toxicants have been treated and even prevented by pharmacological levels of Zn. In ruminants, siliceous forages ingested contribute to soluble siliceous materials in rumen fluid that bind to Cu, Mn and Zn, thereby decreasing their bioavailability in the lower gastrointestinal tract. Deficiencies of Zn and other trace elements have been elicited by prolonged, unsupplemented total parenteral nutrition and by massive supplements of Fe. An increasing volume of biomedical literature has documented alterations in porphyrin biochemistry and metabolism associated with relatively low-level exposures to dietary and environmental toxicants and xenobiotics, including the trace elements Pb, As, Ga, Mn, Co, Ni and Cu. Some nutrient x toxicant interactions pose negative effects or overt adversity from nutritional supplementation that otherwise would be regarded as totally beneficial, e.g., Fe overload exacerbates the porphyria induced by dioxin, and Fe deficiency lends protection. Similarly, Zn supplementation exacerbated hyperbilirubinemia and other manifestations of hepatotoxicity in sheep caused by toxicants in the plant Kochia scoparia. Recently researchers at the University of Illinois caused As toxicosis in animals by providing excessive cysteine or ascorbic acid in diets containing normally used levels of arsenical compounds widely used as feed additives for swine and poultry. The levels of dietary Se that lead to symptoms of deficiency or of toxicity may be modified greatly by interactions with other nutrients or xenobiotics. Adequacy or inadequacy of trace element nutrients may be altered by xenobiotics in beverages such as tea, or by pharmaceuticals such as cimetidine or even non-prescription antacids. containing soluble aluminum. Whether boron is a required nutrient or merely interacts with nutrients to provide benefits is a topic of current interest. Both requirements and tolerances of trace elements are modified by interactions with other nutrients and xenobiotics. Research to elucidate these interactions promises to improve animal and human health and to increase productivity of livestock.