Tissue response to a supplement high in aluminum and silicon.

The objective was to determine the effects of sodium zeolite A (SZA) on mineral metabolism and tissue mineral composition in calves. Twenty calves were placed on study at 3 days of age and were placed into one of two groups: SS, which received 0.05% BW SZA added to their milk replacer, and CO, which received only milk replacer. Blood samples were taken on days 0, 30, and 60 for mineral analysis. Urine and feces were collected on day 30 for mineral metabolism, and on day 60, the calves were euthanized, and samples were taken from numerous organs for mineral analyses. Aluminum retention was increased in the SS calves (p = 0.001). Silicon concentrations were increased in the aorta, spleen, lung, muscle, and kidney of the SS calves, and aluminum was increased in all SS tissues (p < 0.05). Calcium concentrations were increased in aorta, liver, muscle, and tendon; phosphorus concentrations were increased in aorta, but decreased in plasma; magnesium concentrations were increased in aorta, heart, kidney, liver, and pancreas, but decreased in plasma; and iron concentrations were decreased in kidney and liver (p < 0.05). The accumulation of tissue aluminum and therefore potential adverse consequences may preclude any benefits of using SZA as a dietary supplement.

Sodium zeolite a supplementation and its impact on the skeleton of dairy calves.

Twenty calves were placed on study at 3 days of age and were placed according to birth order into one of two groups: SS, which received 0.05% BW sodium zeolite A (SZA) added to their milk replacer, and CO, which received only milk replacer. Blood samples were taken on days 0, 30, and 60 for osteocalcin (OC) and deoxypyridinoline (DPD) analysis. On day 60, the calves were euthanized, and synovial fluid, articular cartilage, and both fused metacarpals were collected for bone quality analyses such as architecture and mechanical properties, mineral composition, and glycosaminoglycan concentration. There were no differences in OC concentrations because of treatment (p = 0.12), and CO calves had lower DPD concentrations than SS calves (p = 0.01), but the OC-to-DPD ratio was not different between treatments (p = 0.98). No differences in bone architecture or mechanical properties were detected. SZA supplementation increased cortical bone (p = 0.0002) and articular cartilage (p = 0.05) aluminum content. Glycosaminoglycan concentrations were not different in synovial fluid or cartilage. Supplementation of SZA appeared to alter the rate of bone turnover without altering bone strength. Aluminum concentrations in the bone and cartilage increased, which may be a concern, although the long-term consequences of such remain to be determined.

Update on the relationship between magnesium and exercise.

Magnesium is involved in numerous processes that affect muscle function including oxygen uptake, energy production and electrolyte balance. Thus, the relationship between magnesium status and exercise has received significant research attention. This research has shown that exercise induces a redistribution of magnesium in the body to accommodate metabolic needs. There is evidence that marginal magnesium deficiency impairs exercise performance and amplifies the negative consequences of strenuous exercise (e.g., oxidative stress). Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20%. Based on dietary surveys and recent human experiments, a magnesium intake less than 260 mg/day for male and 220 mg/day for female athletes may result in a magnesium-deficient status. Recent surveys also indicate that a significant number of individuals routinely have magnesium intakes that may result in a deficient status. Athletes participating in sports requiring weight control (e.g., wrestling, gymnastics) are apparently especially vulnerable to an inadequate magnesium status. Magnesium supplementation or increased dietary intake of magnesium will have beneficial effects on exercise performance in magnesium-deficient individuals. Magnesium supplementation of physically active individuals with adequate magnesium status has not been shown to enhance physical performance. An activity-linked RNI or RDA based on long-term balance data from well-controlled human experiments should be determined so that physically active individuals can ascertain whether they have a magnesium intake that may affect their performance or enhance their risk to adverse health consequences (e.g., immunosuppression, oxidative damage, arrhythmias).

Effects of a diet low in copper on copper-status indicators in postmenopausal women.

To study the effects of low copper intake in older individuals, 12 postmenopausal women, aged 63.1 +/- 8.8 y, were fed a diet containing 9 micromol (0.57 mg) Cu/d for 105 d, followed by a copper-repletion period of 35 d during which the diet was supplemented with 31.5 micromol (2.0 mg) Cu/d. Plasma copper and ceruloplasmin did not change significantly during copper depletion but ceruloplasmin decreased during copper repletion. Erythrocyte superoxide dismutase activity dropped significantly during low copper intake from 3450 to 2600 U/g hemoglobin, but did not increase during copper repletion. Platelet cytochrome c oxidase activity changed significantly (P<0.0001) from 1740 to 810 U/g protein during copper depletion, then increased to 1000 U/g protein during copper repletion. Erythrocyte glutathione peroxidase activity responded similarly. Clotting factor VIII activity increased significantly during copper depletion, then dropped during copper repletion. Low copper intakes did not induce the changes in serum cholesterol and hematology generally found in copper-deficient animal models. These results indicate that a paradigm shift may be needed in evaluating copper status in adult humans. Sensitive indicators of copper include functional activities of platelet cytochrome c oxidase, platelet copper, glutathione peroxidase, and clotting factor VIII. Plasma copper, ceruloplasmin, and cholesterol are relatively insensitive indicators. Also, the recovery from mild copper depletion may require more aggressive intervention tha 2 mg Cu/d for 35 d.

Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations.

Findings from animal studies indicate that dietary boron affects several aspects of mineral metabolism, especially when animals are subjected to nutritional stressors. Eleven postmenopausal volunteers living on a metabolic ward for 167 d (one 23-d equilibration period and six 24-d treatment periods) were fed a conventional basal diet that supplied a daily average intake of 0.36 mg B, 109 mg Mg, and < 0.10 mg A1/8400 kJ. They were given supplements of 0 (BB) or 3 mg B (SB, last two periods only), 0 (BMg) or 200 mg Mg (SMg) (with magnesium supplements held constant during the last two periods), or 0 (BAl) or 1000 mg A1 (SAl)/d. The SB treatment, compared with the BB treatment, provided a 9.0-fold increase in dietary boron but yielded only a 1.5-fold increase in plasma boron concentrations. Regardless of boron dietary treatment, fecal plus urinary excretion of boron accounted for nearly 100% of dietary boron intake with no evidence of boron accumulation over time. Lack of boron accumulation and relatively small changes in blood boron values during a substantial increase in dietary boron support the concept of boron homeostasis. In subjects fed BMg, SB decreased the percentage of dietary calcium lost in the urine but increased that percentage in volunteers fed SMg, a relation that may be important in understanding metabolic mineral disorders that perturb calcium balance. Reduced calcium absorption during SAl suggests that aluminum supplementation should be limited or at least monitored in postmenopausal women prone to excessive calcium loss. Decreased total urinary oxalate during SB in BMg subjects indicates a possible role for boron in the control of urolithiasis during low-magnesium nutriture.

Changes in dietary zinc and copper affect zinc-status indicators of postmenopausal women, notably, extracellular superoxide dismutase and amyloid precursor proteins.

BACKGROUND: Zinc is an essential trace element for human health and well-being; however, methods currently available for the assessment of zinc status in humans are unsatisfactory. OBJECTIVE: The objective was to critically evaluate the use of various indicators of zinc status in humans in a controlled metabolic ward study. DESIGN: Indicators of zinc status were measured in 25 healthy postmenopausal women aged 64.9 +/- 6.7 y. After a 10-d equilibration period, volunteers consumed a diet with either a low (1 mg/d; n = 12) or a high (3 mg/d; n = 13) copper content based on a total energy content of 8.4 MJ. They received the same amount of copper throughout the study. Both groups were fed the basal diet (3 mg Zn/d) with no zinc supplement for one 90-d period, and the diet supplemented with 50 mg Zn/d for another 90-d period. RESULTS: Zinc supplementation significantly increased (P < 0.0001) extracellular but not erythrocyte superoxide dismutase activity. This increase was more apparent when subjects were fed the low-copper diet. Zinc supplementation in combination with the low-copper diet significantly decreased (P < 0.01) amyloid precursor protein expression in platelets. Other indicators of zinc status that were significantly elevated after zinc supplementation were as follows: plasma zinc and free thyroxine concentrations and mononuclear 5'-nucleotidase activity. CONCLUSION: The measurement of serum extracellular superoxide dismutase activity may be useful as a marker for the functional assessment of zinc status in humans.

Ascorbic acid: effect on ongoing iron absorption and status in iron-depleted young women.

The effect of ascorbic acid on iron retention from a diet with predicted low iron bioavailability (containing minimal meat and ascorbic acid) was investigated in iron-depleted premenopausal women. Eleven women were depleted of storage iron (indicated by serum ferritin) through a combination of diet (5.0 mg Fe/2000 kcal for 67-88 d) and phlebotomy. They then consumed a diet containing 13.7 mg Fe/2000 kcal, supplemented with placebo or ascorbic acid three times daily (1500 mg total) with meals for 5.5 wk. Ascorbic acid improved apparent iron absorption (balance method) [38 +/- 2% (means +/- SEM) vs 27 +/- 2%]. Ascorbic acid also improved hemoglobin, erythrocyte protoporphyrins, and serum iron but not hematocrit, serum ferritin, iron-binding capacity, or transferrin saturation. In iron-depleted women consuming a diet with predicted poor iron availability, ascorbic acid supplementation enhanced body iron retention for 5.5 wk.

Selected ultratrace elements in total parenteral nutrition solutions.

Ultratrace elements are potentially essential (eg. boron, molybdenum, nickel, and vanadium) or toxic (eg, aluminum and cadmium) in humans. Long-term total parenteral nutrition (TPN) patients can inadvertently receive significant amounts of ultratrace elements present as contaminants in TPN solutions. We determined the intake of selected ultratrace elements from a standard TPN solution and compared it with the amount reported to be absorbed from food in normal subjects. Contamination of TPN solutions with ultratrace elements was widespread and variable. The daily intakes of Mo, Ni, V. and Cd from this contamination were comparable to the amounts reported to be absorbed through the gastrointestinal tract in normal subjects. Al intake was high; B intake was low, approximately 10% of the amount absorbed by normal subjects. Thus, TPN solutions are contaminated with significant amounts of ultratrace elements. The biological significance of the intravenous infusion of these ultratrace elements is unclear and requires further investigation, particularly in home TPN patients.

Intake of nickel and vanadium by humans. A survey of selected diets.

The nickel and vanadium contents of nine institutional diets were determined by atomic absorption spectrometry with background correction. The following values were obtained for nickel: mean concentration, 0.27 +/- 0.02 microgram/g (dry weight); range, 0.19 and 0.41 microgram/g; mean intake, 165 +/- 11 microgram/day or 75 +/- 10 microgram/1000 cal. The respective values for vanadium were: 0.032 +/- 0.004 microgram/g (dry weight); 0.019 to 0.050 microgram/g; 20.4 +/- 2.3 microgram/day or 8.9 +/- 1.0 microgram/1000 cal. Thus, vanadium is present at approximately one order of magnitude less than nickel.

Biochemical and physiologic consequences of boron deprivation in humans.

Boron deprivation experiments with humans have yielded some persuasive findings for the hypothesis that boron is an essential nutrient. In the first nutritional study with humans involving boron, 12 postmenopausal women first were fed a diet that provided 0.25 mg boron/2000 kcal for 119 days, and then were fed the same diet with a boron supplement of 3 mg boron/day for 48 days. The boron supplementation reduced the total plasma concentration of calcium and the urinary excretions of calcium and magnesium, and elevated the serum concentrations of 17 beta-estradiol and testosterone. This study was followed by one in which five men over the age of 45, four postmenopausal women, and five postmenopausal women on estrogen therapy were fed a boron-low diet (0.23 mg/2000 kcal) for 63 days, then fed the same diet supplemented with 3 mg boron/day for 49 days. The diet was low in magnesium (115 mg/2000 kcal) and marginally adequate in copper (1.6 mg/2000 kcal) throughout the study. This experiment found higher erythrocyte superoxide dismutase, serum enzymatic ceruloplasmin, and plasma copper during boron repletion than boron depletion. The design of the most recent experiment was the same as the second study, except this time the diet was adequate in magnesium and copper. Estrogen therapy increased plasma copper and serum 17 beta-estradiol concentrations; the increases were depressed by boron deprivation. Estrogen ingestion also increased serum immunoreactive ceruloplasmin and erythrocyte superoxide dismutase; these variables also were higher during boron repletion than depletion for all subjects, not just those ingesting estrogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Interactions between essential trace and ultratrace elements.

Fully crossed, factorially arranged experiments showed that, under defined conditions, interactions occur between nickel and iron, nickel and copper, arsenic and zinc, and possibly vanadium and chromium. Nickel and iron interacted when dietary iron was supplemented as ferric sulfate only. Signs of nickel deprivation were more severe when dietary iron was low; or the signs of moderate iron deficiency were more severe when dietary nickel was deficient. When iron was supplemented to the diet as a 60% ferric-40% ferrous sulfate mixture, nickel and iron apparently did not interact. The findings suggested a synergistic relationship between nickel and iron when dietary iron was in a relatively unavailable form. An antagonistic interaction between nickel and copper was found when dietary iron was supplemented as a 60% ferric-40% ferrous sulfate mixture. Signs of copper deficiency were more severe in nickel-supplemented than in nickel-deprived rats. When the rats were made severely iron deficient by feeding of low levels of ferric sulfate only, no apparent interaction between nickel and copper was found. The interaction between arsenic and zinc apparently was noncompetitive. When dietary zinc was 40 microgram/g, arsenic-deprived chicks exhibited depressed growth and elevated hematocrits. In zinc deficiency, growth was more markedly depressed and hematocrits more markedly elevated in arsenic-supplemented than in arsenic-deficient chicks. Arsenic might be necessary for the efficient utilization or metabolism of zinc. Findings indicating an interaction between vanadium and chromium were tentative. In one experiment, the addition of 500 microgram of chromium/g of diet apparently made 5 micrograms of vanadium/g of diet toxic for chicks. Thus, the interactions between essential trace and ultratrace elements might be of nutritional significance.

A moderately high intake compared to a low intake of zinc depresses magnesium balance and alters indices of bone turnover in postmenopausal women.

OBJECTIVES: To determine whether moderately high or low intakes of zinc adversely affect the copper status of postmenopausal women to result in unfavorable changes in calcium and magnesium metabolism and other indicators of bone turnover. DESIGN: After a 10-day equilibration period in which the diet provided 31.5 micromol (2 mg) Cu and 137.7 micromol (9 mg) Zn/8.4 MJ (2000 kcal), the subjects were randomly divided into two groups, with one group fed the basal diet supplemented to provide 15.7 micromol (1 mg) Cu/8.4 MJ, and the other group fed the same diet supplemented to provide 47.2 micromol (3 mg) Cu/8.4 MJ. After equilibration, both groups were fed the basal diet with no zinc supplemented (provided 45.9 micromol [3 mg] Zn/8.4 MJ) for 90 days; this was followed by another 10-day equilibration period before the basal diet was supplemented with zinc to provide 811 micromol (53 mg)/8.4 MJ for 90 days. SETTING: The metabolic unit of the Grand Forks Human Nutrition Research Center, Grand Forks, ND, USA. SUBJECTS: A total of 28 postmenopausal women recruited by advertisement throughout the United States of America. Among them, 25 women (64.9+6.7 y) completed the study; 21 as designed. RESULTS: The moderately high intake compared to the low intake of zinc increased the excretion of magnesium in the feces and urine, which resulted in a decreased magnesium balance. In the women fed low dietary copper, plasma osteocalcin was higher during the low-zinc than high-zinc dietary period. The urinary excretion of N-telopeptides was increased and the serum calcitonin concentration was decreased by high dietary zinc regardless of dietary copper. CONCLUSIONS: A moderately high intake of zinc (811 micromol/day; 53 mg/day) did not induce changes in copper metabolism that resulted in unfavorable changes in bone or mineral metabolism. However, low dietary zinc (45.9 micromol/day; 3 mg/day) apparently resulted in undesirable changes in circulating calcitonin and osteocalcin. As a moderately high intake of zinc decreased magnesium balance, further study of the possibility that a high intake of zinc is a health concern for individuals consuming less than the recommended amounts of magnesium is warranted.

Low dietary zinc alters indices of copper function and status in postmenopausal women.

OBJECTIVES: To better define the relationship between dietary zinc and copper for humans so that sound recommendations for intakes of these elements can be made. METHODS: A study was conducted to ascertain the effect of moderately excessive and deficient intakes of zinc on copper metabolism and use in humans fed low and luxuriant amounts of copper. Twenty-one postmenopausal women housed in a metabolic unit completed the study as designed. After a 10-d equilibration period in which they were fed a diet providing 31.5 micromol (2 mg) Cu and 91.8 micromol (9 mg) Zn/8.4 MJ (2000 kcal), the women were divided into two groups. One group was fed a diet containing 15.7 micromol (1 mg) Cu/8.4 MJ (2000 kcal), and the other group was fed a diet containing 47.2 micromol (3 mg) Cu/8.4 MJ (2000 kcal). After equilibration, both groups were fed the basal diet providing 45.9 micromol (3 mg) Zn/8.4 MJ (2000 kcal) for 90 d; this was followed by another 10-d equilibration period before dietary zinc was increased to 811 micromol (53 mg)/8.4 MJ (2000 kcal) for 90 d. RESULTS: The women were in positive copper balance only when the diet provided 47.2 micromol (3 mg) Cu and 811 micromol (53 mg) Zn/d. Immunoreactive ceruloplasmin concentrations and platelet cytochrome-c oxidase activity on a platelet number basis were significantly lower and the ratio between enzymatic and immunoreactive ceruloplasmin was significantly higher during low dietary than during high dietary zinc intake. Serum cholesterol was higher in subjects fed 15.7 micromol (1 mg) Cu/d than in those fed 47.2 micromol (3 mg) Cu/d. Total and low-density lipoprotein cholesterol concentrations decreased with zinc supplementation. Whole-blood glutathione concentration and erythrocyte glutathione peroxidase activity were lower during high than during low dietary zinc intake. CONCLUSIONS: The findings indicate that an inadequate intake of zinc (45.9 micromol/d; 3 mg/d) was more effective than a moderately high intake of zinc (811 micromol/d; 53 mg/d) in inducing changes associated with a decreased copper status in postmenopausal women. Furthermore, the findings indicate that copper status indicators might be useful in evaluating changes in zinc status in humans, and an intake of 15.7 micromol (1 mg)/d of copper may be inadequate for postmenopausal women.

New essential trace elements for the life sciences.

The possible importance of some new essential trace elements in nutrition is discussed. Most likely, insufficient intake of a specific trace element becomes obvious only when the body is stressed in some way that enhances the need for that element; this has been supported by recent findings with selenium. The trace elements boron and copper may be of nutritional significance in a manner similar to selenium. When the diets of animals and humans are manipulated to cause possible changes in cellular integrity or in hormone responsiveness, a large number of responses to dietary boron occur. The findings indicate that boron is important for optimal calcium and, thus, bone metabolism. High dietary cystine and fructose exacerbate the signs of copper deficiency in rats; this indicates that the response to copper deficiency by humans would vary with the amino acid and carbohydrate composition of the diet. There is some evidence that chromium, molybdenum, nickel, arsenic, and vanadium may also be of nutritional significance under stress conditions. In other words, an increasing number of studies have been performed that have examined the importance of trace element nutriture in various forms of nutritional, metabolic, hormonal, or physiologic stress in animals and humans. These studies indicate that situations will be found in which a trace element is of nutritional significance. It is likely that some of the trace elements are more important in human nutrition than is now generally acknowledged.

The justification for providing dietary guidance for the nutritional intake of boron.

Because a biochemical function has not been defined for boron (B), its nutritional essentiality has not been firmly established. Nonetheless, dietary guidance should be formulated for B, because it has demonstrated beneficial, if not essential, effects in both animals and humans. Intakes of B commonly found with diets abundant in fruits, vegetables, legumes, pulses, and nuts have effects construed to be beneficial in macromineral, energy, nitrogen, and reactive oxygen metabolism, in addition to enhancing the response to estrogen therapy and improving psychomotor skills and cognitive processes of attention and memory. Perhaps the best-documented beneficial effect of B is on calcium (Ca) metabolism or utilization, and thus, bone calcification and maintenance. The paradigm emerging for the provision of dietary guidance that includes consideration of the total health effects of a nutrient, not just the prevention of a deficiency disease, has resulted in dietary guidance for chromium (Cr) and fluoride; both of these elements have beneficial effects in humans, but neither has a defined biochemical function. Knowledge of B nutritional effects in humans equals or is superior to that of Cr and fluoride; thus, establishing a dietary reference intake for B is justified. An analysis of both human and animal data suggests that an acceptable safe range of population mean intakes of B for adults could well be 1-13 mg/d. Recent findings indicate that a significant number of people do not consistently consume more than 1 mg B/d; this suggests that B could be a practical nutritional or clinical concern.

Effect of form of iron on nickel deprivation in the rat: Plasma and liver lipids.

In two fully-crossed, two-factor, completely randomized experiments, female weanling rats were fed a basal diet (containing about 10 ng of nickel and 2.3 µg of iron/g) supplemented with graded levels of nickel and iron. Iron was supplemented to the diet in experiment 1 at levels of 0, 25, 50, and 100 µg/g as a mixture of 40% FeSO4·nH2O and 60% Fe2(SO4)3·nH2O and in experiment 2 at levels of 0, 12.5, 25, 50, and 100 µg/g as Fe2(SO4)3·nH2O. In both experiments, nickel was supplemented to the diet at levels of 0, 5, and 50 µg/g as NiCl2·3H2O. Regardless of dietary nickel, rats fed no supplemental iron exhibited depressed levels of plasma phospholipids and elevated levels of liver total lipids. Nickel deprivation elevated plasma and liver total lipids in rats fed supplemental ferric sulfate only. When dietary iron was supplied as a ferric-ferrous sulfate mixture, nickel deprivation depressed plasma, and did not affect liver total lipids. However, within each experiment nickel and iron did not interact to affect plasma and liver total lipids or phospholipids. The findings suggest that the effect of dietary nickel on plasma and iver lipids of rats is influenced by the form of dietary iron.

Effects in rats of iron on lead deprivation.

In two fully crossed, two-factor experiments, F1 generation male rats were fed a basal diet supplemented with lead (lead acetate) at 0 or 2 micrograms/g and iron (ferric sulfate) at 50 or 250 micrograms/g (Experiment 1). Supplements in Experiment 2 were lead at 0 or 1 micrograms/g and iron at 50, 250, or 1000 micrograms/g. After 28 or 50 d in Experiment 1, and 35 d in Experiment 2, a relationship between lead and iron was found. Body weight was lower in low-lead than lead-supplemented 28-d-old rats regardless of dietary iron, whereas hematocrit and hemoglobin were lower in low-lead than lead-supplemented rats fed 50 micrograms iron/g diet. A similar finding was obtained with hematocrit and hemoglobin in 35-d-old rats. Dietary lead did not affect rats fed 250 or 1000 micrograms iron/g diet. Also, feeding low dietary lead did not affect 50-d-old rats regardless of dietary iron. Liver and bone concentrations of lead were markedly affected by dietary lead and iron. The concentration of lead in liver and bone was lower in low-lead than lead-supplemented rats. Compared to rats fed 50 micrograms iron/g diet, rats fed 250 micrograms iron/g diet exhibited a decreased lead concentration in liver and bone. This decrease was accentuated by lead supplementation. The findings suggest that lead acted pharmacologically to affect iron metabolism in rats.

Effects in chicks of arsenic, arginine, and zinc and their interaction on body weight, plasma uric acid, plasma urea, and kidney arginase activity.

The interaction among arsenic, zinc, and arginine was studied in chicks using two fully crossed, three-way, two-by-two-by-two experiments. Arsenic at levels of 0 and 2 µg/g zinc at levels of 2.5 (zinc-deficient) and 25 (zinc-adequate) µg/g, and arginine at levels of 0 and 16 mg/g were supplemented to the diet. After 28 d in both experiments, growth was depressed in chicks fed diets either supplemented with arginine or deficient in zinc. Arsenic deprivation depressed growth of chicks fed diets containing the basal level of arginine and 25 µg supplemental Zn/g. Arsenic deprivation had little or no effect on growth of zinc-deprived chicks fed diets containing the basal level of arginine, or in zinc-deprived or zinc-adequate chicks fed supplemental arginine. Zinc-deficiency elevated urea in plasma and arginase activity in kidney. Those elevations, however, were more marked in arsenic-supplemented than in arsenic-deprived chicks. Also, plasma urea and kidney arginase activity were markedly elevated in chicks fed supplemental arginine; the elevations were more marked in zinc-deficient chicks. These findings support the concept that arsenic has a physiological role, associated with zinc, that can influence arginine metabolism in the chick.

Studies of the interaction between boron and calcium, and its modification by magnesium and potassium, in rats. Effects on growth, blood variables, and bone mineral composition.

Two experiments were performed to confirm that boron interacts with calcium, and that this interaction can be modified by dietary magnesium and potassium in the rat. Upon manipulating the dietary variables listed above, it was found that under certain conditions, boron and calcium deprivation similarly affected several variables; for example, they both could be made to elevate plasma alkaline phosphatase activity and to depress femur calcium concentration. Under some dietary conditions, both boron and calcium deprivation affected some variables related to blood or iron metabolism. However, the effects of dietary boron and calcium on spleen weight/body weight ratio, hematocrit, and femur iron concentration generally were not similar. Femur copper, magnesium, phosphorus, and zinc also were affected by an interaction between boron and calcium under some dietary conditions. The findings show that there is a relationship between boron and calcium, but they do not clearly indicate the nature of the relationship. However, the data suggest that boron and calcium act on similar systems in the rat.

Dietary silicon and arginine affect mineral element composition of rat femur and vertebra.

Both arginine and silicon affect collagen formation and bone mineralization. Thus, an experiment was designed to determine if dietary arginine would alter the effect of dietary silicon on bone mineralization and vice versa. Male weanling Sprague-Dawley rats were assigned to groups of 12 in a 2 x 2 factorially arranged experiment. Supplemented to a ground corn/casein basal diet containing 2.3 microg Si/g and adequate arginine were silicon as sodium metasilicate at 0 or 35 microg/g diet and arginine at 0 or 5 mg/g diet. The rats were fed ad libitum deionized water and their respective diets for 8 wk. Body weight, liver weight/body weight ratio, and plasma silicon were decreased, and plasma alkaline phosphatase activity was increased by silicon deprivation. Silicon deprivation also decreased femoral calcium, copper, potassium, and zinc concentrations, but increased the femoral manganese concentration. Arginine supplementation decreased femoral molybdenum concentration but increased the femoral manganese concentration. Vertebral concentrations of phosphorus, sodium, potassium, copper, manganese, and zinc were decreased by silicon deprivation. Arginine supplementation increased vertebral concentrations of sodium, potassium, manganese, zinc, and iron. The arginine effects were more marked in the silicon-deprived animals, especially in the vertebra. Germanium concentrations of the femur and vertebra were affected by an interaction between silicon and arginine; the concentrations were decreased by silicon deprivation in those animals not fed supplemental arginine. The change in germanium is consistent with a previous finding by us suggesting that this element may be physiologically important, especially as related to bone DNA concentrations. The femoral and vertebral mineral findings support the contention that silicon has a physiological role in bone formation and that arginine intake can affect that role.