Interaction between nickel and iron in the rat

The interaction between nickel and iron was confirmed in rat metabolism. In a fully-crossed, two-way, three by four, factorially designed experiment, female weanling rats were fed a basal diet supplemented with iron at 0, 25, 50, and 100 μg/g and with nickel at 0, 5, and 50 μg/g. The basal diet contained about 10 ng of nickel and 2.3 μg of iron/g. After nine weeks, dietary iron affected growth, hematocrit, hemoglobin, plasma cholesterol, and in liver affected total lipids, phospholipids, and the contents of copper, iron, manganese, and zinc. By manipulating the iron content of the diet, effects of dietary nickel were shown in rats that were not from dams fed a nickel-deprived diet. Nickel affected growth, hematocrit, hemoglobin, plasma alkaline phosphatase activity, plasma total lipids, and in liver affected total lipids, and the contents of copper, manganese, and nickel. The interaction between nickel and iron affected hematocrit, hemoglobin, plasma alkaline phosphatase activity, and plasma phospholipids, and in liver affected size, content of copper, and perhaps of manganese and nickel. In severely iron-deficient rats, the high level of dietary nickel partially alleviated the drastic depression of hematocrit and hemoglobin, and the elevation of copper in liver. Simultaneously, high dietary nickel did not increase the iron level in liver and was detrimental to growth and appearance of severely iron-deficient rats. In nickel-deprived rats fed the borderline iron-deficient diet (25 μg/g) hematocrit and hemoglobin also were depressed. However, 5 μg Ni/g of diet were just as effective as 50 μg Ni/g of diet in preventing those signs of nickel deprivation. The findings in the present study suggested that nickel and iron interact with each other at more than one locus.     

Effect of dietary nickel and iron on the trace element content of rat liver

The level and/or form of dietary iron, dietary nickel, and the interaction between them affected the trace element content of rat liver. Livers were from the offspring of dams fed diets containing 10–16 ng, or 20 μg, of nickel/g. Dietary iron was supplied as ferric chloride (30 μg/g) or ferric sulfate (30 μg, or 60 μg). In nickel-deprived rats fed 60 μg of iron/g of diet as ferric sulfate, at age 35 days, levels of iron and zinc were depressed in liver and the level of copper was elevated. At age 55 days, iron was still depressed, copper was still elevated, but zinc also was elevated. In rats fed 30 μg of iron/g of diet as ferric chloride, liver iron content was higher in nickel-deprived than in nickel-supplemented rats at 30, but not at 50, days of age. Also manganese and zinc were lower in nickel-deprived than in nickel-supplemented rats at age 35 days if their dams had been on experiment for an extended period of time (i.e., since age 21 days). Thus, the levels of copper, iron, manganese, and zinc in liver were affected by nickel deprivation, but the direction and extent of the affects depended upon the iron status of the rat.     

Interactions among nickel,copper, and iron in rats

In two fully-crossed, three-way, two-by-three-by-three, factorially arranged experiments, female weanling rats were fed a basal diet supplemented with iron at 15 and 45 μg/g, nickel at 0, 5, and 50 μg/g, and copper at either 0, 0.5, and 5 μ/g (Expt. 1) or 0, 0.25, and 12 μg/g (Expt. 2) A gram of basal diet contained in Expt. 1 approximately 16 ng of nickel, 2.3 μg of iron, and 0.47 μg of copper; and in Expt. 2, 20 ng of nickel, 1.3 μg of iron, and 0.39 μg of copper. Expt. 1 was terminated at 11 weeks, and Expt. 2 at 8 weeks because, at those times, some rats fed no supplemental copper and the high level of nickel began to lose weight, or die from heart rupture. The findings demonstrated that relationships are complex among nickel, copper, and iron. Nickel interacted with copper and this interaction was influenced by dietary iron. Signs of copper deficiency were more severe when nickel was supplemented to the diet provided that copper deprivation was neither very severe nor mild. Iron deprivation apparently enhanced the antagonism by exacerbating copper deficiency. Signs of copper deficiency that were made more severe by nickel supplementation were depressed weight gain (Expt. 2), hematocrit (Expt. 1), hemoglobin, and plasma alkaline phosphatase activity; and elevated ratios of heart wt/body wt, kidney wt/body wt, and liver wt/body wt. Because nickel and copper have similar physical and chemical properties, the interactions between those two elements were probably the result, of isomorphous replacement of copper by nickel at various functional sites that interfered with some biological processes.     

Anemia associated with changes in iron and iron-59 utilization in copper deficient rats fed high levels of dietary ascorbic acid and iron

The influence of dietary copper, iron, and ascorbic acid on iron utilization was examined in a 2×2×2 factorial experiment. Male Sprague-Dawley weanling rats were fed copper-deficient (Cu-, 0.42 μg Cu/g) or copper-adequate (Cu+, 5.74 μg Cu/g) diets that contained one of two levels of iron (38 or 191μg Fe/g) and ascorbic acid (0 or 1% of the diet). These eight diets were fed for 20 d, and rats received an oral dose of 4 μCi iron-59 on d 15. Compared to Cu+ rats, the Cu− rats had 27% lower hemoglobin levels with 45, 59, and 65% lower cytochrome c oxidase (CCO) activities in the liver, heart, and bone marrow, respectively (p<0.0001). High dietary iron or ascorbic acid did not alter hemoglobin in Cu+ rats. However, hemoglobin was 23% lower in Cu− rats fed the highest, rather than the lowest levels of iron and ascorbic acid. Liver CCO was decreased (p<0.02) in Cu− rats fed high iron. Among Cu− rats, ascorbic acid did not influence CCO but decreased hemoglobin by 17% (p<0.001), reduced the percentage of absorbed iron-59 in the erythrocytes by 91% (p<0.05) and depressed the percentage apparent absorption of iron (p<0.05). These results suggest that the effects of elevated dietary iron and ascorbic acid on iron utilization are influenced by copper status.     

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.     

Effect of form of iron on nickel deprivation in the rat

In three fully crossed, factorially arranged, 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; in experiment 2 at levels of 0, 12.5, 25, 50, and 100 μg/g as Fe₂(SO₄)₃·nH₂O; in experiment 3 at levels of 0, 25, and 50 μg/g as either the mixture of ferric-ferrous sulfates, or as ferric sulfate only. Nickel as NiCl₂·3H₂O was supplemented to the diet in experiment 1 at levels of 0, 5, and 50 μg/g; in experiment 2 at levels of 0 and 50 μg/g; and in experiment 3 at levels of 0 and 5 μg/g. Regardless of dietary nickel, rats fed no supplemental iron exhibited depressed iron content and elevated copper, manganese, and zinc contents in the liver. Nickel and iron did not interact to affect iron, manganese, and zinc in liver. Liver copper was inconsistently affected by an interaction between nickel and iron. Nickel deprivation apparently accentuated the elevation of the copper level in livers of severely iron-deficient rats. Experiment 3 showed that the form of dietary iron altered the effect of nickel deprivation on the iron content of the liver. When only ferric sulfate was supplemented to the diet, liver iron content was depressed in nickel-deprived rats. On the other hand, when the ferric-ferrous mixture was supplemented to the diet, nickel deprivation apparently elevated the iron content in the liver. The findings support the views that (1) parameters that are affected by an interaction between nickel and iron are limited in factorially arranged experiments, and (2) the form and level of dietary iron markedly influence the effect of nickel deprivation in the rat.     

Interactions among vanadium,iron, and cystine in rats growth,blood parameters,and organ Wt/body Wt ratios

In three fully crossed, three-way, two-by-two-by-four experiments, male weanling Long-Evans rats were fed a basal diet supplemented with vanadium (ammonium metavanadate)-at 0 and 1 μg/g, cystine at 3.0 and 8.5 mg/g, and iron (ferric sulfate) at 0 (Expts. 1 and 2) or 5 (Expt. 3), 15, 100, and 500 μg/g. After 6 wk, a relationship between vanadium and iron that was influenced by dietary cystine was found. The interaction among vanadium, iron, and cystine was demonstrated best by the hematocrit and hemoglobin findings, which were similar. In all Expts., hematocrits were depressed in rats fed the two lower levels of iron. In Expts. 2 and 3, vanadium deprivation exacerbated the depression of hematocrits in rats fed 15 μg iron and 3.0 mg cystine/g diet. In Expt. 1, the effect was similar, but less marked. On the other hand, in Expts. 1 and 3 when supplemental cystine was 8.5 mg/g, vanadium deprivation did not exacerbate, but tended to alleviate the depression of hematocrits in rats fed 15 μg iron/g diet. When dietary iron was 15 μg/g in Expt. 2, the exacerbation of the depression of hematocrits by vanadium deprivation was much less in rats fed 8.5 rather than 3.0 mg cystine/g diet. Dietary vanadium had little effect on depressed hematopoiesis in severely iron-deficient rats. The findings indicated that vanadium neither substitutes for iron at some metabolic site, nor stimulates iron absorption; but has a positive influence on the utilization of iron after absorption.     

Dietary vitamin B12, sulfur amino acids,and odd-chain fatty acids affect the response of rats to nickel deprivation

An experiment was performed to ascertain whether changing the dietary intake of two substances, cystine and margaric acid (heptadecanoic acid), that affect the flux through pathways involving the two vitamin B₁₂-depednent enzymes, methionine synthase and methylmalonyl-CoA mutase, would affect the interaction between nickel and vitamin B₁₂. Rats were assigned to treatment groups of six in a fully crossed, four-factorial arrangement. The independent variables, or factors, were: per kg of fresh diet, nickel analyzed at 25 and 850 μg; vitamin B₁₂ supplements of 0 and 50 μg; margaric acid supplements of 0 and 5 g; andl-cystine supplements of 0 and 12 g. The diet without cystine was marginally deficient in sulfur amino acids. Nickel affected growth, liver wt/body wt ratio (LB/BW), and a number of variables associated with iron, calcium, zinc, copper, and magnesium metabolism. Most of the effects of nickel were modified by the vitamin B₁₂ status of the rat. In numerous cases, the interaction between nickel and vitamin B₁₂ was dependent on, or altered by, the cystine or margaric acid content of the diet. Thus, the findings showed that the extent and the direction of changes in numerous variables in response to nickel deprivation varied greatly with changes in diet composition. These variables include those previously reported to be affected by nickel deprivation, including growth and the distribution or functioning of iron, calcium, zinc, copper, and magnesium. The findings also support the hypothesis that nickel has a biological function in a metabolic pathway in which vitamin B₁₂ is important.     

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 2×2 factorially arranged experiment. Supplemented to a ground corn/casein basal diet containing 2.3 μg Si/g and adequate arginine were silicon as sodium metasilicate at 0 or 35 μg/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. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area is an equal opportunity/affirmative action employer, and all agency services are available without discrimination. Mention of a trademark or proprietary product does not constitute a guarantee or warranty of the product by the U.S. Department of Agriculture and does not imply its approval to the exclusion of other products that may be suitable.     

Serum and liver zinc,copper, and iron in chicks infected withEimeria acervulina orEimeria tenella

Two-wk-old broiler chicks were inoculated via crop intubation withEimeria acervulina at two doses: 10⁵ or 10⁶ sporulated oocysts/bird or withEimeria tenella at a dose of 10⁵ sporulated oocysts/bird. Serum and liver samples were collected on days 3 and 6 post-inoculation (PI). There were no significant changes in serum or liver zinc, copper, and iron concentrations in any of the infected groups by 3 d PI. However, on d 6, PI serum protein was significantly reduced in all of the infected groups compared to their pair-fed controls. The chicks infected withE. tennella had significantly reduced serum zinc (1.20 vs 1.77 μg/mL) and iron (0.44 vs 1.28 μg/mL) concentrations and significantly elevated serum copper (0.28 vs 0.17 μg/mL) and ceruloplasmin levels (20.33 vs 11.11 μg/mL) compared to their pair-fed counterparts. Those chicks infected withE. acervulina (10⁶ oocysts/bird) exhibited significantly reduced serum iron concentration by 6 days PI (0.90 vs 1.14 μg/mL). Liver zinc was significantly increased in the chicks infected withE. tenella (349 vs 113 μg/g dry liver wt), as was copper (24 vs 19 μg/g), whereas liver iron concentration was significantly reduced (172 vs 243 μg/g) compared to pair-fed controls. At both dose levels, the chicks infected withE. acervulina exhibited a significant reduction in liver iron by 6 d PI. Hepatic cytosol metals generally reflected whole tissue levels. Metallothionein (MT)-bound zinc was significantly elevated in the chicks infected withE. tenella. Iron bound to a high molecular weight, heat-stable protein fraction (presumably cytoplasmic ferritin) was significantly reduced in chicks infected withE. acervulina, as well as those infected withE. tenella. Collectively, the changes in serum zinc, copper, and iron concentrations, as well as the changes in hepatic zinc and MT-zinc concentrations in the chicks infected withE. tenella were similar to changes evoked during an acute phase response to infection. It is possible that a secondary bacterial infection or inflammation stemming from erosion of the lining of the cecum may play a role in the response of trace element metabolism to theE. tenella infection. Mentions of a trademarkr, proprietary product or specific equipment does not consitute a guarantee or warranty by the US Department of Agriculture and does not imply its approval to the exclusion of other products.     

Effects of germanium and silicon on bone mineralization

The chemical properties of Ge are similar to Si. This study investigated whether Ge can substitute for, or is antagonistic to, Si in bone formation. Sixty male weanling Sprague-Dawley rats were randomly assigned to treatment groups of 12 and 6 in a 2×4 factorially arranged experiment. The independent variables were, per gram fresh diet, Si (as sodium metasilicate) at 0 or 25 μg and Ge (as sodium germanate) at 0, 5, 30 or 60 μg. Results confirmed that Ge does not enhance Si deprivation and provided evidence that Ge apparently can replace Si in functions that influence bone composition. When Si was lacking in the diet, calcium and magnesium concentrations of the femur were decreased; this was reversed by feeding either Ge and/or Si. Similar effects were found for zinc, sodium, iron, manganese, and potassium of vertebra. There were some responses to Si deprivation that Ge could not reverse: Ge did not increase femur copper, sodium, or phosphorus or decrease molybdenum of vertebra, effects that were eveked by Si supplementation. Additionally, some findings suggested that 60 μg Ge/g diet could be a toxic intake for the rat. On the other hand, some responses induced by Ge indicate that this element may be acting physiologically other than as a substitute for Si. Germanium itself affected bone composition. Germanium supplementation decreased Si and molybdenum in the femur and increased DNA in tibia. Regardless of the amount of Si fed, animals fed 30 μg Ge/g diet had increased tibial DNA compared to animals fed 0 or 60 μg Ge; however, tibial DNA of animals fed 30 μg Ge was not statistically different from those animals fed 5 μg Ge. Thus, Ge may be of nutritional importance.     

Magnesium and methionine deprivation affect the response of rats to boron deprivation

A series of nine experiments were done to obtain further evidence that boron might be involved in major mineral metabolism (Ca, P, and Mg), thus indicating that boron is an essential nutrient for animals. Eight factorially arranged experiments of 6–10 wk durations were done with weanling Sprague-Dawley male rats. One factorially arranged experiment was done with weanling spontaneously hypertensive rats. The variables in each experiment were dietary boron supplements of 0 and 3 μg/g, and dietary magnesium supplements of either 200 (Experiments 1–3) or 100 (Experiments 4–9) and 400 μg/g. In Experiments 7 and 9, a third variable was dietary manganese supplements of 25 and 50 μg/g. Methionine status was varied throughout the series of experiments by supplementing the casein-based diet with methionine and arginine. Findings were obtained indicating that the severity of magnesium deprivation and the methionine status of the rat strongly influence the extent and nature of the interaction between magnesium and boron, and the response to boron deprivation. When magnesium deprivation was severe enough to cause typical signs of deficiency, a significant interaction between boron and magnesium was found. Generally, the interaction was characterized by the deprivation of one of the elements making the deficiency signs of the other more marked. The interaction was most evident when the diet was not supplemented with methionine and especially when the diet contained luxuriant arginine. Signs of boron deprivation were also more marked and consistent when the diet contained marginal methionine and luxuriant arginine. Among the signs of boron deprivation exhibited by rats fed marginal methionine were depressed growth and bone magnesium concentration, and elevated spleen wt/body wt and kidney wt/body wt ratios. Because the boron supplement of 3 μg/g did not make the dietary intake of this element unusual, it seems likely that the response of the rats to dietary boron in the present study were manifestations of physiological, not pharmacological, actions, and support the hypothesis that boron is an essential nutrient for the rat. Mentions of a trademark or proprietary product does not consitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable.     

Copper status in rats fed diets supplemented with either vitamin E,vitamin A,or β-carotene

Copper status was measured in rats fed copper-adequate, purified diets supplemented with either vitamin E (250 IU/kg), vitamin A (40,000 IU/kg), or β-carotene (2 g/kg). It was hypothesized that the extra intake of the antioxidants would spare vitamin C resulting in a decreased copper status as shown previously after supplementation with vitamin C. A significant increase in plasma ascorbate concentration was observed after β-carotene supplementation, but not after supplemental vitamin E or vitamin A. Extra intake of either β-carotene or vitamin A slightly, but significantly, raised plasma copper concentrations. β-carotene also slightly raised liver copper concentration. Supplemental vitamin E had no effect on plasma and liver copper concentrations. It is concluded that the observed relatively small effects of supplemental vitamin A and β-carotene on copper status in rats are not mediated by changes in plasma vitamin C concentration.     

The pH dependence of siliconiron interaction in rats

A 2 x 2 x 3 factorial experiment was conducted to study the pH dependence of a silicon-iron interaction in vivo. The dietary treatments used in the factorial design were the following (mg/kg of diet): silicon, 0 and 500; iron, 35 and 187; acid-base, ammonium chloride as 0.5% of total diet (acidic), sodium bicarbonate as 1.0% of total diet (basic), or no supplementation of acid or base (control). The supplementation of 500 mg silicon/kg of diet increased plasma-iron concentration in rats fed the acidic or control diets, but not in rats fed the basic diet. A high dietary-iron level suppressed copper absorption and utilization and subsequently imposed a negative effect on its own utilization. An increase in the plasma total-cholesterol concentration caused by high dietary-iron level was likely a consequence of the antagonistic effect of iron on copper absorption and utilization. The use of cupric sulfate pentahydrate as the dietary-copper source in this study resulted in plasma copper concentrations that were approximately twice those obtained in a related study using cupric carbonate. Also, a 42% coefficient of variation (C.V.) for plasma-copper concentrations of rats fed cupric sulfate in this study was greatly reduced from the C.V. = 108% previously associated with the dietary cupric carbonate.     

Nickel deficiency diminishes sperm quantity and movement in rats

Early studies on nickel essentiality with rats and goats indicated that nickel deprivation impaired reproductive performance. Nickel also has been found to influence cyclic nucleotide gated channels (CNG); these types of channels are important in sperm physiology. Thus, two experiments were conducted to test the hypothesis that nickel deficiency affects sperm physiology in a manner consistent with nickel having an essential function related to CNG channel functions. The experiments were factorially arranged with four treatment groups of eight weanling rats in each. In experiment 1, the treatments were supplemental dietary nickel of 0 and 1 mg/kg and N ^ω -nitro-l-arginine methyl ester (l-NAME, a nitric oxide synthase inhibitor) added to the drinking water (50 mg/100 mL) the last 3 wk of an 8-wk experiment. In experment 2, the treatments were supplemental dietary nickel at 0 and 1 mg/kg and supplemental dietary sodium chloride (NaCl) at 0 and 80 g/kg. The NaCl and l-NAME variables were included to act as stressors affecting CNG channel activity. The basal diet contained per kilogram about 27 μg of nickel and 1 g of sodium. After 8 wk in experiment 1 and 16 wk in experiment 2, urine while fasting and testes and epididymis in both experiments, and seminal vesicles and prostates in experiment 2 were harvested for analysis. Nickel deprivation significantly decreased spermatozoa motility and density in the epididymides, epididymal transit time of spermatozoa, and testes sperm production rate. Nickel deficiency also significantly decreased the weights of the seminal vesicles and prostate glands. Excessive NaCl had no effect on sperm physiology; however, it decreased prostate gland weights. The findings support the hypothesis that nickel has an essential function that possibly could affect reproductive performance in higher animals, perhaps through affecting a CNG channel function. Part of the data was presented at the Experimental Biology 2001 Meeting, Orlando, FL, March 31–April 4, 2001. (F. H. Nielsen, E. O. Uthus and K. Yokoi, Dietary nickel deprivation decreases sperm motility and evokes hypertension in rats, FASEB J. 15, A972 (2001), and K. Yokoi, E. O. Uthus and F. H. Nielsen, Nickel deficiency induces renal damages and hypertension in rats which is augmented by sodium chloride, FASEB J. 15, A973 (2001). The US Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination. Mention of a trademark or proprietary product does not constitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of the products that may also be suitable.     

Effect of dietary copper and zinc levels on tissue copper,zinc, and iron in male rats

The interaction between dietary copper and zinc as determined by tissue concentrations of trace elements was investigated in male Sprague-Dawley rats. Animals were fed diets in a factorial design with two levels of copper (0.5, 5 μg/g) and five levels of zinc (1, 4.5, 10, 100, 1000 μg/g) for 42 d. In rats fed the low copper diet, as dietary zinc concentration increased, the level of copper decreased in brain, testis, spleen, heart, liver, and intestine. There was no significant effect of dietary copper on tissue zinc levels. In the zinc-deficient groups, the level of iron was higher in most tissues than in tissues from controls (5 μg Cu, 100 μg Zn/g diet). In the copper-deficient groups, iron concentration was higher than control values only in the liver. These data show that dietary zinc affected tissue copper levels primarily when dietary copper was deficient, that dietary copper had no effect on tissue zinc, and that both zinc deficiency and copper deficiency affected tissue iron levels.     

Biochemical interactions among silicon, iron and ascorbic acid in the rat

A 2 x 2 x 2 factorial experiment was conducted using two dietary levels each (mg/kg of diet) of silicon, 0 and 500; iron, 35 and 187; and ascorbic acid, 0 and 900, to identify biochemical interactions occurring among these nutrients. Supplemental silicon, in conjunction with the higher dietary-iron level, prevented the plasma-iron decreasing effect observed for the higher level of iron in the absence of silicon. In the absence of ascorbic acid, silicon also increased iron concentration in the liver. Lower growth of the silicon and iron-supplemented rats is believed to be a response to a subsequent iron-imposed aberration of copper or zinc metabolism. This is supported by decreased intestinal metallothionein, increased weights (g/100 g body weight) of liver, heart, and testes, and decreased packed-cell volume and hemoglobin concentration. The lower plasma-iron level associated with the higher level of dietary iron appeared to be an expression of the iron-imposed reduction of liver copper stores. Ascorbic acid decreased plasma-iron concentration and prevented the silicon-related increase in liver iron.     

Intestinal iron absorption in chickens

Intestinal iron absorption in chickens was studied in vivo, using an intestinal perfusion technique in closed circuit. The results obtained show that iron absorption, at 30 min intervals, is a linear function of test solution iron concentrations of up to 776 μg Fe/20 mL. At higher concentrations, iron saturation occurs. The mucosal epithelial cells seem to be less a limiting factor than in rats. However, in chickens, the binding capacity of plasma might play an important role in the regulation of iron absorption. Iron absorption versus time was analyzed in 15, 30, 60, and 120 min periods for the iron concentration of 14 μg Fe/20 mL. Intestinal iron absorption showed a linear relationship between these two parameters. A period of perfusion of either 30 or 60 min by a solution of 14 μg Fe/20 mL appears suitable since no interference by a saturation process can then occur.     

Effect of iron and/or vitamin A re-supplementation on vitamin A and iron status of rats after a dietary deficiency of both components

Iron and vitamin A deficiency are common nutritional problems in developing countries. From animal experiments and intervention studies, growing evidence is pointing to a possible influence of iron on vitamin A metabolism. We assessed the affects of an oral supplementation of vitamin A and/or iron on the recovery of rats from vitamin A and iron deficiency. Weanling male Wistar rats were kept for four weeks on an iron and vitamin A deficient diet. Thereafter, rats were repleted with iron 35 mg/kg feed, with vitamin A 4500 IU/kg feed both, or with iron 35 mg/kg and vitamin A 4500 IU/kg for five weeks. Retinol and retinyl esters in plasma and tissues were determined by HPLC. Iron was determined by atomic absorption spectrophotometry. The determination of haematological parameters showed that rats developed an anaemia during depletion. This was reversed by the re-supplementation with iron but not vitamin A alone. The simultaneous supplementation of vitamin A was of no additional benefit. When rats were resupplemented with iron alone a substantial further decrease in plasma retinol (P < 0.002) and liver vitamin A (P < 0.05) was observed. A similar but less pronounced decrease in plasma retinol was observed in the rats re-supplemented with vitamin A alone, despite a substantial increase in liver vitamin A (P < 0.002). Despite lower liver vitamin A levels compared to the group re-supplemented with vitamin A lone, the group re-supplemented with iron and vitamin A had substantial higher plasma levels compared to the one supplemented with iron alone (P < 0.002). In conclusion, the study supports an interaction of iron and vitamin A on the level of retinol transport in plasma. Despite a comparable availability of vitamin A as indicated by the comparable liver levels only the re-supplementation of both iron and vitamin A can normalize the retinol level in plasma. This might be of nutritional consequence in developing countries with regard to the supplementation regime of both nutrients iron and vitamin A to prevent a functional deficiency of vitamin A despite sufficient dietary availability.     

Induction of metallothionein in rat tissues following subchronic exposure to mercury shown by radioimmunoassay

Although the analysis of metallothionein (MT) by radioimmunoassay (RIA) is not a common technique, its use is preferred over other methods since it offers the advantages of sensitivity and specificity. In this paper we present data on the basal levels of MT in rat tissues and physiological fluids of female Sprague-Dawley rats. The mean basal MT concentrations of the following organs and fluids were determined by RIA to be: liver (9.8 μg/g), kidney (68 μ/g), brain (0.8 μg/g), spleen (1.0 μg/g), heart (5.4 μg/g), plasma (11 ng/ml), and urine (200–300 μg/g creatinine). Following subcutaneous exposure to inorganic mercury (0.2 μmol/kg/d, 5 d a week for up to 4 wk), the metal accumulated primarily in the kidney. There was also a simultaneous accumulation of zinc in the liver and of zinc and copper in the kidney. Induction of MT did take place in liver, kidney, brain, and spleen. No increases in the MT contents of blood and urine were noted. The excess zinc and copper in the kidney of exposed animals were found to be associated predominantly with MT. No overt signs of mercury toxicity were noted in these animals and the incidence of proteinurea was nil. The data are discussed with reference to methods of MT determination in animal tissues and in relation to mercury metabolism and toxicity.