Advances in metal-induced oxidative stress and human disease

Chapter 1: Overview of Zinc Nutrition ............................................................................................................... S99 1.1 Biological functions of zinc ............................................................................................................................. S99 1.2 Tissue zinc distribution and reserves .............................................................................................................. S99 1.3 Zinc metabolism ........................................................................................................................................... S100 1.4 Importance of zinc for human health........................................................................................................... S101 1.5 Human zinc requirements............................................................................................................................. S105 1.5.1 Adult men ............................................................................................................................................. S106 1.5.2 Adult women......................................................................................................................................... S109 1.5.3 Children ................................................................................................................................................ S110 1.5.4 Pregnancy.............................................................................................................................................. S111 1.5.5 Lactation ............................................................................................................................................... S112 1.6 Dietary sources of zinc and suggested revisions of Recommended Daily Intakes .................................... S112 1.6.1 Dietary sources of zinc and factors affecting the proportion of zinc available for absorption ........ S112 1.6.2 Revised estimates of dietary requirements and recommended intakes for zinc ............................... S114 1.7 Zinc toxicity.................................................................................................................................................... S118 1.8 Causes of zinc deficiency and groups at high risk ....................................................................................... S121 1.9 Summary ........................................................................................................................................................ S123

International Zinc Nutrition Consultative Group (IZiNCG) technical document #1. Assessment of the risk of zinc deficiency in populations and options for its control.

Trace elements in human physiology and pathology: zinc and metallothioneins.

Compared to several other metal ions with similar chemical properties, zinc is relatively harmless. Only exposure to high doses has toxic effects, making acute zinc intoxication a rare event. In addition to acute intoxication, long-term, high-dose zinc supplementation interferes with the uptake of copper. Hence, many of its toxic effects are in fact due to copper deficiency. While systemic homeostasis and efficient regulatory mechanisms on the cellular level generally prevent the uptake of cytotoxic doses of exogenous zinc, endogenous zinc plays a significant role in cytotoxic events in single cells. Here, zinc influences apoptosis by acting on several molecular regulators of programmed cell death, including caspases and proteins from the Bcl and Bax families. One organ where zinc is prominently involved in cell death is the brain, and cytotoxicity in consequence of ischemia or trauma involves the accumulation of free zinc. Rather than being a toxic metal ion, zinc is an essential trace element. Whereas intoxication by excessive exposure is rare, zinc deficiency is widespread and has a detrimental impact on growth, neuronal development, and immunity, and in severe cases its consequences are lethal. Zinc deficiency caused by malnutrition and foods with low bioavailability, aging, certain diseases, or deregulated homeostasis is a far more common risk to human health than intoxication.

https://www.mdpi.com/1660-4601/7/4/1342/pdf

The Essential Toxin: Impact of Zinc on Human Health

Publisher Summary This chapter discusses that the knowledge of phytic acid had its beginning in the discovery by Hartig, who isolated small particles or grains (which were not starch grains) from the seeds of various plants. Phytic acid has been generally regarded as the primary storage form of both phosphate and inositol in almost all seeds. The amount of phytic acid varies from 0.50% to 1.89% in cereals (except polished rice), from 0.40% to 2.06% in legumes, from 2.00% to 5.20% in oil seeds except soybeans and peanuts (grouped under legumes), and from 0.40% to 7.50% in protein products. Many foods and seeds contain myo-inositol hexaphosphate as an important source of phosphorus, and accurate methods for its determination are needed. Phytase (meso-inositol hexaphosphate phosphohydrolase, EC 3.1.3.8) is widely distributed in plants, animals, and fungi. In mature cereal grains, legumes, and oil seeds, the major portion of the total phosphorus is present in the form of phytic acid (phytate). Experiments with animals have suggested that phytic acid in plant foods complexes with dietary essential minerals such as calcium, zinc, iron, and magnesium and makes them biologically unavailable for absorption. The correlation of phytate with the cooking quality of peas was first suggested by Mattson. Phytic acid, myo-inositol 1,2,3,4,5,6-hexakis dihydrogen phosphate serves as the main phosphorus store in mature seeds and grains. In cereals and legumes, phytic acid content ranges from 0.14% to 2.05%, which accounts for 18 to 88% of the total phosphorus.

Phytates in Legumes and Cereals

Zinc metabolism in patients with the syndrome of iron deficiency anemia, hepatosplenomegaly, dwarfism, and hypognadism.

Introduction A syndrome consisting of iron-deficiency anemia, hepatosplenomegaly, dwarfism, and hypogonadism occurring in males in Iran has been described recently by Prasad, Halsted, and Nadimi. 1,2 To account for all the features of the syndrome, it was suggested in the earlier report that these patients were probably zinc deficient. Subsequently, similar patients were studied in Egypt and were found to be zinc deficient. 16 The purpose of this paper is to present results of extensive biochemical studies in such patients, to characterize more fully the nature of this syndrome, and to describe five cases in detail. Clinical Material and Methods Patients were selected from villages near Cairo. The ages, verified by birth certificate in each case, ranged from 12 to 19 years. None of them had any evidence of chronic infections such as tuberculosis, syphilis, or brucellosis. A detailed history and physical examination were carried out on each patient on

Biochemical studies on dwarfism, hypogonadism, and anemia.

Zinc and iron deficiencies in male subjects with dwarfism and hypogonadism but without ancylostomiasis, schistosomiasis or severe anemia.

Zinc, iron, and nitrogen content of sweat in normal and deficient subjects.

Clinical and experimental. Zinc metabolism in patients with the syndrome of iron deficiency anemia, hepatosplenomegaly, dwarfism, and hypogonadism. 1963.

A. Miale

Papers

Zinc metabolism in patients with the syndrome of iron deficiency anemia, hepatosplenomegaly, dwarfism, and hypognadism.

Biochemical studies on dwarfism, hypogonadism, and anemia.

Zinc and iron deficiencies in male subjects with dwarfism and hypogonadism but without ancylostomiasis, schistosomiasis or severe anemia.

Zinc, iron, and nitrogen content of sweat in normal and deficient subjects.

Clinical and experimental. Zinc metabolism in patients with the syndrome of iron deficiency anemia, hepatosplenomegaly, dwarfism, and hypogonadism. 1963.