Metabolism trace elements

Iyengar, G.V., Kasperek, K. and Feinendegen, LE. (1978) Retention of the metabolized trace elements in biological tissues following drying procedures. I. Antimony, cobalt, iodine, mercury, selenium and zinc in rat tissues. Sci. Tot. Environ., 10,1-16. 

It appears that chromium(III) is an essential trace element in mammalian metabolism and, together with insulin, is responsible for the clearance of glucose from the blood-stream. Tungsten too has been found to have a role in some enzymes converting CO2 into formic acid but, from the point of view of biological activity, the focus of interest in this group is unquestionably on molybdenum. 

Electrolytes, vitamins, and trace elements are essential for numerous biochemical and metabolic functions and should be added to PN daily unless otherwise not indicated. 

In summary, we may add that bacterial utilization of quinoline and its derivatives as a rule depends on the availability of traces of molybdate in the culture medium [363], In contrast, growth of the bacterial strains on the first intermediate of each catabolic pathway, namely, the lH-2-oxo or 1 II-4-oxo derivatives of the quinoline compound was not affected by the availability of molybdate. This observation indicated a possible role of the trace element molybdenum in the initial hydroxylation at C2. In enzymes, Mo occurs as part of the redox-active co-factor, and all the Mo-enzymes involved in N-heteroatomic compound metabolism, contain a pterin Mo co-factor. The catalyzed reaction involves the transfer of an oxygen atom to or from a substrate molecule in a two-electron redox reaction. The oxygen is supplied by the aqueous solvent. Certainly, the Mo-enzymes play an important role in the initial steps of N-containing heterocycles degradation. 

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. 

Richards, M.R 1989a. Recent developments in trace element metabolism and function role of metallothionein in copper and zinc metabolism. Jour. Nutr. 119 1062-1070. 

Goals of nutrition support include correcting caloric and nitrogen imbalances, fluid or electrolyte abnormalities, and vitamin or trace element abnormalities, without causing or worsening other metabolic complications. 

Both macronutrients (i.e., water, protein, dextrose, and IV fat emulsion [IVFE]) and micronutrients (i.e., vitamins, trace elements, and electrolytes) are necessary to maintain normal metabolism. 

Knowles, S.O. and Donaldson, W.E., Lead disrupts eicosanoid metabolism, macrophage function, and disease resistance in birds, Biol. Trace Element Res. 60, 13, 1997. 

As the human body is able to store many minerals, deviations from the daily ration are balanced out over a given period of time. Minerals stored in the body include water, which is distributed throughout the whole body calcium, stored in the form of apatite in the bones (see p. 340) iodine, stored as thyroglobulin in the thyroid and iron, stored in the form of ferritin and hemosiderin in the bone marrow, spleen, and liver (see p. 286). The storage site for many trace elements is the liver. In many cases, the metabolism of minerals is regulated by hormones—for example, the uptake and excretion of H2O, Na, ... 

In humans, the major pathway in the metabolism of the thyroid hormones consists of the removal of iodine or deiodination. Three deiodinase isoenzymes, encoded on three distinct genes, catalyze the reductive deiodination. All three enzymes contain the rare amino acid seleno-cysteine. The essential trace element selenium therefore plays an important role in thyroid hormone economy. 

It is an essential trace element for mammals, but little is known about its role or requirement in human metabolism. In humans, serum levels of nickel are about 1.1 to 1.6 mcg/1. This level increases in conditions such as stroke and acute myocardial infarction. A dietary requirement for adults is about 30 meg/day. 

Selenium is an essential trace element in the human body. This nutrient is an important part of antioxidant enzymes that protect cells against the effects of free radicals that are produced during normal oxygen metabolism. Selenium is also essential for normal functioning of immune system and thyroid gland. 

The unusual physical complaints and findings in workers overexposed to tellurium include somnolence, anorexia, nausea, perspiration, a metallic taste in the mouth and garlic-like odor on the breath (48). The unpleasant odor, attributed to the formation of dimethyltelluride, has not been associated with any adverse health symptoms. Tellurium compounds and metabolic products have been identified in exhaled breath, sweat, urine, and feces. Elimination is relatively slow and continuous exposure may result in some accumulation. No definite pathological effects have been observed beyond the physical complaints outlined. Unlike selenium, tellurium has not been proved to be an essential biological trace element. 

Heavy metals stimulate or inhibit a wide variety of enzyme systems (16, 71, 72), sometimes for protracted periods (71, 73). These effects may be so sensitive as to precede overt toxicity as in the case of lead-induced inhibition of 8 ALA dehydrase activity with consequential interference of heme and porphyrin synthesis (15, 16). Urinary excretion of 8 ALA is also a sensitive indicator of lead absorption (74). Another erythrocytic enzyme, glucose-6-phosphatase, when present in abnormally low amounts, may increase susceptibility to lead intoxication (75), and for this reason, screens to detect such affected persons in lead-related injuries have been suggested (76). Biochemical bases for trace element toxicity have been described for the heavy metals (16), selenium (77), fluoride (78), and cobalt (79). Heavy metal metabolic injury, in addition to producing primary toxicity, can adversely alter drug detoxification mechanisms (80, 81), with possible secondary consequences for that portion of the population on medication. 

Prasad, A. S. 1978. Trace Elements and Iron in Human Metabolism. Plenum Medical Book Co., New York. 

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