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In experiments on rats, a significant influence of an extraordinarily high bromide intake on the whole-body biological half-life of iodine was established. Very high bromide intake (1) decreased the amount of radioiodide accumulated in the thyroid, (2) changed the proportion between the amount of iodine retained in the thyroid and the total amount of absorbed iodine, (3) significantly shortened the biological half-life of iodine in the thyroid from approximately 101 h to 33 h in animals maintained on an iodine-sufficient diet and from 92 h to about 30 h in rats fed a low-iodine diet, and (4) changed the time-course (added a further phase) of iodine elimination from the body. These changes were caused, with high probability, by an increase of iodine elimination by kidneys due to an excess of bromide. The overall picture of iodine elimination in animals fed the low-iodine diet was similar to that in animals maintained on iodine-sufficient diet.

The effect of a high bromide intake on the kinetics of iodide uptake and elimination in the thyroid and skin of adult male rats was studied. In rats fed a diet with sufficient iodine supply (> 25 microg I/d), the iodide accumulation in the skin predominated during the first hours after 131I iodide application. From this organ, radioiodide was gradually transferred into the thyroid. A high bromide intake (> 150 mg Br-/d) in these animals led to a marked decrease in iodide accumulation, especially by the thyroid, because of an increase in iodide elimination both from the thyroid and from the skin. In rats kept under the conditions of iodine deficiency (< 1 micro I/d), the iodide accumulation in the thyroid, but not in the skin, was markedly increased as a result of a thyrotropic stimulation. The effect of a high bromide intake (> 100 mg Br-/d) in these animals was particularly pronounced because the rates of iodide elimination were most accelerated both from their thyroid and from their skin.

The biological half-life of bromine in the rat thyroid was determined by measuring the radioactivity of thyroids of animals which continuously received 82Br labelled bromide in their food. The value of this half-life (110 h) is practically the same as the biological half-life of iodine. The rate of establishing the I/Br concentration ratio in the thyroid depends on the biological half-life of bromine. The mechanism of this process depends on the state of iodine supply. When the supply is sufficient, the iodine concentration in the thyroid remains constant, while during iodine deficiency the iodine atoms are replaced by atoms of bromine.

The time course of iodine excretion in adult male rats substantially differs from bromine excretion. Bromine is excreted at a single rate, whereas iodine evinces two excretion rates. Even a strong increase in bromide intake in experimental animals failed to affect the rate of iodine excretion but it lowered the fraction of iodine accumulated in the thyroid gland by 20% probably by affecting the transport of iodide into the thyroid gland.

In experiments with rats, we have found that at enhanced intake of bromide, bromine does not replace chlorine in the thyroid; it replaces iodine. Under our experimental conditions, more than one-third of the iodine content in the thyroid was replaced by bromine. In the thyroid, bromine probably remained in the form of bromide and, in proportional to its increased concentration, the production of iodinated thyronines decreased, with the sum of the iodine and bromine concentrations being constant at the value of 20.51 +/- 1.16 mumol/g dry wt of the thyroid. In contrast to other organs, the biological behavior of bromine in the thyroid is not similar to the biological behavior of chlorine but resembles more that of iodine.

The beneficial effects of a combined dietary supplement of Zn, Cu, and Mn in decreasing Cd absorption was previously reported. The purpose of this study was to investigate the individual and combined effects of these three elements. In the first two experiments, day-old Japanese quail were fed basal diets containing either requirement amounts of Zn (30 ppm) and Mn (12 ppm) and slightly above requirement levels of Cu (5 ppm). From Day 7 birds were fed either the basal diet or diets containing combinations at twice these concentrations; a 2 X 2 X 2 factorial design was used. 109Cd content and Cd concentration of these diets were 100 mu Ci and 145 micrograms/kg, respectively. In the third experiment, day-old birds were fed either the basal diet or a basal diet containing 109Cd and single additional supplements of either Zn, Cu, or Mn. All birds were killed at 14 days of age. The Cd concentration was determined for the duodenum, jejunum-ileum, liver, and kidney. When the experimental diets were fed for 7 days, only Zn had a protective effect against Cd. Whereas none of the elements reduced the Cd concentration of the duodenum, Zn reduced the Cd in the jejunum-ileum, liver, and kidney by approximately 66, 21, and 11%, respectively. Cu and Mn caused occasional increases of Cd in some tissues. Feeding the experimental diets for 2 weeks resulted in similar responses. Zn nutrition appears to play an important role in protecting against dietary Cd absorption.

Male Wistar rats were treated with Mo in a single dose or over a period of 84 days. The course of molybdenum excretion after a single dose was expressed mathematically. It was shown that various tissues produced different excretion curves and a high retention was observed only in skin. In long-term treatment it was possible to ascribe this retention to direct binding of molybdenum to collagen. In contrast to some other heavy metals molybdenum causes a decrease of collagen stability. The mechanism of this effect is discussed.

This study describes the interaction of molybdenum with blood components. Molybdenum-99 was added to blood, and after four washings, 3% of the total radioactivity was found in red cells. More specifically, the radioactivity was determined to be associated with the cell membrane.Molybdenum-99 in the +VI form did not interact with the human erythrocyte membrane; however, Mo(V) forms did interact. Of five different compounds, the highes uptake was observed with a brown Mo(V)-ascorbate complex generated from Mo(VI) and ascorbic acid in the molar ratio 1∶20. A membrane suspension of Mo-ascorbate-treated human erythrocytes was prepared and the solubilized proteins were separated on a polyacrylamide gel in the presence of sodium dodecyl sulfate (SDS). Molybdenum-99 binding to spectrin was demonstrated, as well as some minor interactions with membrane hemoglobin and bands 6 and 8.

The interaction of 99Mo with red cell membrane proteins was found specific for spectrin both in normal red cells and those of hereditary spherocytosis. In addition, no significant quantitative differences were observed in labeling patterns between these two types of red cells, thus indicating no major alterations in the spectrin molecules of hereditary spherocytosis.

Molybdenum belongs to a group of essential microelements and occurs in all components of the environment. Major Mo sources for man are foods, especially vegetable, to a lesser extent drinking water. Its metabolism is primarily influenced by interaction with other metals, specifically copper and iron. In the organism it is primarily accumulated in the liver, kidneys, skin and hard tissues. In the blood it binds specifically with alpha-2-macroglobulin, in the erythrocytic membrane with spectrin; it enhances the osmotic resistance of red blood cells. From the organism it is eliminated in the urine, bile and feces. The biochemical importance of molybdenum lies in that it catalyzes the oxidation of xanthine and purine bases and the reduction of nitrates and molecular nitrogen; it is also present in the prosthetic group of flavoprotein enzymes. As shown in both epidemiological and animal studies, molybdenum ions may prevent dental caries. Long-term overexposure to Mo may produce molybdenosis (teart) in cattle. Increased exposures of humans may be primarily encountered in the foundry industry, but the toxic manifestations are invariably nonspecific, similarly as in the case of other heavy metals. Molybdenum-exposed workers may also show elevated uric acid concentrations in their blood, simultaneously with clinical symptoms resembling gout (gout-like syndrome). A similar finding may also occur among individuals living in areas characterized by elevated molybdenum and decreased copper contents in soil. The maximum allowable concentration limits established for soluble and insoluble molybdenum compounds in the workplace air have been accepted in many countries, but their values vary in a wide range. No specific exposure test for molybdenum has been developed as yet.

The radioactive labeling of spectrin using the pentavalent complex of molybdenum-99 was applied to the study of membrane protein in pyruvate kinase deficient red cells. Compared to the control, the labeling profile of the enzymopathic red cell membrane proteins remained generally unchanged but the molybdenum uptake was found to depend largely on the reticulocyte count. This finding may reflect changes during the cell maturation.

The effect of in vivo administration of molybdenum (as sodium molybdate) and tungsten (as sodium tungstate) was investigated in the skin of laboratory rats. It was proved that the amount of both bound molybdenum and tungsten in collagen is relatively small being 0.05 and 0.06 moles per mole respectively. Besides the fraction of firmly bound molybdenum and tungsten a much higher extractable pool of both these metals was found. It was also demonstrated that in vivo shadowing of collagen is caused by the fraction of loosely bound metals. On the other hand pronounced changes were shown in the mechanical properties of connective tissue after molybdate and tungstate administration. Surprisingly, the change in mechanical properties indicated a lower level of cross-linking after the administration of the investigated metals. It is therefore concluded that bitopical binding of molybdenum and tungsten in the collagen structure is unlikely. It also appears that the biological effect of these metals is due to the competition with copper and the interference with the physiological cross-linking reactions based on the partial blockade of lysyloxidase.