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.     

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.     

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 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.     

Effects of copper, iron, and ascorbic acid on manganese availability to rats.

Four experiments were done to characterize the interactions of copper, iron, and ascorbic acid with manganese in rats. All experiments were factorially arranged Dietary Mn concentrations were less than 1 micrograms/g (Mn0) and 50 micrograms/g (Mn+). Dietary Cu was less than 1 mg/g (Cu0) and 5 micrograms/g (Cu+); dietary Fe was 10 micrograms/g (Fe10) and 140 micrograms/g (Fe140). Ascorbic acid (Asc) was not added to the diet or added at a concentration of 10 g/kg diet. Experiment 1 had two variables, Mn and Cu; in Experiment 2, the variables were Mn and Asc. In Experiment 3, the variables were Mn, Cu, and Asc; in Experiment 4, they were Mn, Cu, and Fe. Definite interactions between Mn and Cu were observed, but they tended to be less pronounced than interactions between Mn and Fe. Cu depressed absorption of 54Mn and accelerated its turnover. In addition, adequate Cu (Cu+), compared with Cu0, depressed liver, plasma, and whole blood Mn of rats. Absorption of 67Cu was higher in animals fed Mn0 diets than in those fed Mn+. Ascorbic acid depressed Mn superoxide dismutase activity and increased Cu superoxide dismutase activity in the heart. The addition of ascorbic acid to the diet did not affect Mn concentration in the liver or blood. Absorption of 54Mn was depressed in rats fed Fe140 compared with those fed Fe10. Interactions among Fe, Cu, and Mn resulted in a tendency for Mn superoxide dismutase activity to be lower in rats fed Fe140 than in rats fed Fe10. Within the physiologic range of dietary concentrations, Mn and Cu have opposite effects on many factors that tend to balance one another. The effects of ascorbic acid on Mn metabolism are much less pronounced than effects of dietary Cu, which in turn affects Mn metabolism less than does Fe.     

Effect of age and dietary protein level on tissue mineral levels in female rats

Mineral (phosphorus, sulfur, potassium, calcium, magnesium, iron, zinc, copper, and manganese) concentrations were measured in plasma, and several tissues from female Wistar rats (young: 3-wk-old; mature: 6-mo-old) were fed on a dietary regimen designed to study the combined or singular effects of age and dietary protein on mineral status. Three diets, respectively, contained 5, 15, and 20% of bovine milk casein. Nephrocalcinosis chemically diagnosed by increased calcium and phosphorus in kidney was prevented in rats fed a 5% protein diet. Renal calcium and phosphorus were more accumulated in young rats than mature rats. A 5% protein diet decreased hemoglobin and blood iron. The hepatic and splenic iron was increased by a 5% protein diet in mature rats but was not altered in young rats. Mature rats had higher iron in brain, lung, heart, liver, spleen, kidney, muscle, and tibia than young rats. A 5% protein diet decreased zinc in plasma and liver. Zinc in tibia was increased with dietary protein level in young rats but was not changed in mature rats. A 5% protein diet decreased copper concentration in plasma of young rats but not in mature rats. Mature rats had higher copper in plasma, blood, brain, lung, heart, liver, spleen, and kidney than young rats. With age, manganese concentration was increased in brain but decreased in lung, heart, liver, kidney, and muscle. These results suggest that the response to dietary protein regarding mineral status varies with age.     

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 0, 0.5, and 5 μg/g (Expt. 1) or 0, 0.25, and 12 μg/g (Expt. 2). 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 experiments showed that nickel interacted with copper and this interaction was influenced by dietary iron. If copper deficiency was neither very severe or mild, copper deficiency signs of elevated levels of total lipids and lipid phosphorus in liver and plasma, and cholesterol in plasma, were made more severe by supplemental dietary nickel. Rats in which nickel supplementation exacerbated copper deficiency did not exhibit a depressed level of copper in liver and plasma. Also, although iron deprivation enhanced the interaction between nickel and copper, iron deprivation did not significantly depress the level of copper in liver and plasma. The findings confirmed that, in rats, a complex relationship exists between nickel, copper, and iron, thus indicating that both the iron and copper status of experimental animals must be controlled before data about nickel nutriture and metabolism can be compared among studies.     

Ascorbic acid reduces the frequency of iron induced micronuclei in bone marrow cells of mice

Iron is a potent oxidant that can lead to the formation of genotoxic lipid peroxides. Ascorbic acid, which enhances dietary iron absorption, has been suggested to enhance the oxidant effects of iron and to directly lead to the formation of lipid peroxides. The combined effects of dietary iron and ascorbic acid on genotoxicity were investigated by measuring the frequency of micronuclei in the bone marrow cells of C3H/He mice. In addition, liver iron concentration was measured in all treated groups. Three weeks old mice were fed diets for 3 weeks containing iron at 100 or 300 mg/kg diet in the form of FeSO(4) that were supplemented either with or without ascorbic acid (15 g/kg diet). The results of the bone marrow micronucleus test revealed that the high iron diet resulted in an increased frequency of micronucleated polychromatic erythrocytes (MnPCEs) as compared to low iron. Ascorbic acid supplementation in the low iron diet did not show any effect on incidence of MnPCEs and protected against the increased frequency of MnPCEs induced by the high iron diet. However, liver iron concentration was significantly increased only in the high iron treated and ascorbic acid supplemented group as compared to all other groups. These results demonstrate that ascorbic acid protects against the clastogenic effects of iron.     

Ascorbic acid reduces the frequency of iron induced micronuclei in bone marrow cells of mice

Iron is a potent oxidant that can lead to the formation of genotoxic lipid peroxides. Ascorbic acid, which enhances dietary iron absorption, has been suggested to enhance the oxidant effects of iron and to directly lead to the formation of lipid peroxides. The combined effects of dietary iron and ascorbic acid on genotoxicity were investigated by measuring the frequency of micronuclei in the bone marrow cells of C3H/He mice. In addition, liver iron concentration was measured in all treated groups. Three weeks old mice were fed diets for 3 weeks containing iron at 100 or 300 mg/kg diet in the form of FeSO₄ that were supplemented either with or without ascorbic acid (15 g/kg diet). The results of the bone marrow micronucleus test revealed that the high iron diet resulted in an increased frequency of micronucleated polychromatic erythrocytes (MnPCEs) as compared to low iron. Ascorbic acid supplementation in the low iron diet did not show any effect on incidence of MnPCEs and protected against the increased frequency of MnPCEs induced by the high iron diet. However, liver iron concentration was significantly increased only in the high iron treated and ascorbic acid supplemented group as compared to all other groups. These results demonstrate that ascorbic acid protects against the clastogenic effects of iron.     

EFFECTS OF DIETARY SUPPLEMENTAL L-CARNITINE AND ASCORBIC ACID ON PERFORMANCE,CARCASS COMPOSITION AND PLASMA L-CARNITINE CONCENTRATION OF BROILER CHICKS REARED UNDER DIFFERENT TEMPERATURE

The present study was initiated to determine whether dietary supplemental L-carnitine and ascorbic acid affect growth performance, carcass yield and composition, abdominal fat and plasma L-carnitine concentration of broiler chicks reared under normal and high temperature. During the experiment, two temperature regimes were employed in two experimental rooms, which were identical but different in environmental temperature. The regimes were thermoneutral (20-22°C for 24 h) or recycling hot (34-36°C for 8 h and 20-22°C for 16 h). One-day-old broiler chicks (ROSS) were used in the experiment. A 2 x 2 x 2 factorial arrangement was employed with two levels (0 and 50 mg/kg) of supplemental L-carnitine and two levels (0 or 500 mg/kg) of supplemental ascorbic acid in drinking water under thermoneutral or high temperature regimes. Body weight gain was affected by high temperature. However, body weight gain was significantly improved in animals receiving supplemental L-carnitine, ascorbic acid or L-carnitine + ascorbic acid compared to animals receiving unsupplemented diet under high temperature. On the other hand, supplemental L-carnitine or L-carnitine + ascorbic acid reduced body weight gain under thermoneutral condition. Supplemental ascorbic acid significantly improved feed conversion efficiency, the improvement was relatively greater under high temperature. The L-carnitine content in the plasma was higher in the groups receiving supplemental L-carnitine and ascorbic acid under high temperature, while broilers fed supplemental L-carnitine and ascorbic acid had a decreased level of plasma L-carnitine concentration under normal temperature. It is concluded that dietary supplemental L-carnitine or L-carnitine + ascorbic acid may have positive effects on body weight gain, carcass weight under high temperature conditions.     

Iron utilization and liver mineral concentrations in rats fed safflower oil, flaxseed oil, olive oil, or beef tallow in combination with different concentrations of dietary iron

Diets with a higher proportion of polyunsaturated fatty acids (i.e., linoleic acid) have decreased iron absorption and utilization compared with diets containing a higher proportion of the saturated fatty acid stearic acid (e.g., beef tallow). However, less is known regarding the influence of other polyunsaturated or monounsaturated fatty acids, along with higher dietary iron, on iron absorption and utilization. The present study was conducted to compare the effects of dietary fat sources known to vary in (n-3), (n-6), and (n-9) fatty acids on iron utilization and liver mineral concentrations. Male weanling rats were fed a diet containing 10, 35, or 100 μg/g iron in combination with saffower oil, flaxseed oil, olive oil, or beef tallow for 8 wk. Indicators of iron status, iron utilization, and liver iron concentrations were unaffected by an interaction between the fat source and iron concentration. Plasma copper was the only variable affected by an interaction between the fat source and dietary iron. Findings of this study demonstrate that flaxseed oil and olive oil may alter tissue minerals and affect iron utilization. Further studies should be conducted to establish the effect of varying (n-3), (n-6), and (n-9) fatty acids on trace mineral status and iron utilization. Data were presented in part at Experimental Biology 2000 as a poster session. A. D. Shotton and E. A. Droke, Dietary fat and iron modify immune function, FASEB J. 14, A239 (2000).     

Chromium and chronic ascorbic acid depletion effects on tissue ascorbate,manganese, and14C retention from14C-ascorbate in guinea pigs

Chromium (Cr) potentiates the effects of insulin and a role for insulin in ascorbic acid transport has been reported. Therefore, the effects of Cr and ascorbate depletion on tissue ascorbic acid and¹⁴C distribution and excretion after a¹⁴C ascorbate dose were investigated in guinea pigs. As utilization of dietary Cr is affected by interaction with other minerals, tissue manganese (Mn), zinc (Zn), copper (Cu), and iron (Fe) were examined. For 20 wk, 40 weanling animals were fed either a Cr-deficient (<0.06 μg Cr/g diet, ?Cr) or a Cr-adequate (2 μg Cr from CrCl₃/g diet, +Cr) casein-based diet and were given 1 mg ascorbate/d (?C) or 10 mg ascorbate/d (+C) for 20 wk. Animals fed the Cr-depleted diet had decreased weight at 20 wk (p<0.01). Six hours before necropsy, animals were dosed by micropipette with 1.8 μCi ofl-[carboxyl-¹⁴C] ascorbic acid and placed in metabolic cages. Ascorbate supplementation increased Fe concentrations in most analyzed tissues, hepatic¹⁴C, tissue ascorbate and Mn concentration in the adrenal and testes, but decreased the concentrations of Cu in the kidney and Mn in the spleen. Liver Mn concentration was higher and kidney Mn concentration was lower in +Cr animals. Interactions between Cr and ascorbic acid affected Mn concentrations in bone and brain. These results indicate that ascorbate and Cr may affect Mn distribution. Chromium supplementation decreased plasma cortisol, brain¹⁴C and the amount of¹⁴C expired as carbon dioxide. These findings suggest that dietary Cr may affect ascorbic acid metabolism and the metabolic response to stress.     

Dietary cadmium decreases lipid peroxidation in the liver and kidneys of the bank vole (Clethrionomys glareolus).

The effect of elevated levels of dietary cadmium on lipid peroxidation in the liver and kidneys of a small rodent, the bank vole, was determined in the present study. Males and females, aged 1 month, were given diets containing 0.40 and 80 mg Cd per kg; liver and kidneys were removed for TBA-RS as well as iron, copper, zinc, cadmium and metallothionein analyses at the end of 6 weeks. Dietary Cd significantly decreased the TBA-RS level in the liver and kidneys of both sexes; however, this effect appeared to be dose-dependent only for the male liver. The changes in hepatic and renal TBA-RS paralleled closely those of tissue iron. Copper concentration decreased significantly only in the male liver, while hepatic and renal zinc were not influenced by dietary Cd. The concentrations of Cd and metallothionein in the liver and kidneys increased significantly in a dose-dependent fashion. Regression analysis confirmed that TBA-RS in both organs correlated closely with iron. The data suggest that dietary Cd decreases hepatic and renal lipid peroxidation indirectly, through lowering the tissue iron concentration.     

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.     

‘Free’ iron, as detected by electron paramagnetic resonance spectroscopy, increases unequally in different tissues during dietary iron overload in the rat

Free iron concentration, as determined by electron paramagnetic resonance (EPR) spectroscopy, and lipid peroxidation (LPO), as determined by thiobarbituric acid test, were assessed in the lung, heart, liver, spleen, brain and kidney of rats subjected to experimental iron overload. Two tests, Desferal- and NO-available iron, were used to measure free iron and gave comparable results. The most pronounced accumulation of free iron was observed in liver, kidney and spleen. Differences between control and iron loaded animals increased during the initial 90 days of treatment. Between 90 and 180 days free iron concentration reached a steady state level, or even decreased, as in the case of liver. Lipid peroxidation level, measured in the organs of both treated and matched controls, did not give any significant difference during the initial 90 days of treatment. A significant augmentation was observed in liver, kidney, spleen and heart at 180 days. The results of the present research show that, under conditions of moderate siderosis, the occurrence of LPO is partially related to the level of free iron.     

Ascorbate is particularly effective against LDL oxidation in the presence of iron(III) and homocysteine/cystine at acidic pH

Metal-catalyzed LDL oxidation is enhanced by the presence of homocysteine. In this study, the effectiveness of ascorbic acid against low-density lipoprotein (LDL) oxidation by iron(III) and copper(II) in the presence of homocysteine and the main plasma disulfide cystine was investigated. Relative to the degree of LDL oxidation reached in the absence of antioxidants, ascorbic acid was particularly effective against iron-catalyzed LDL oxidation at pH 6.0. This can be explained from its stability under acidic conditions and is likely to be important in ischemia, in inflammation and exhausting exercise. At pH 7.4, an ascorbic acid concentration at least as high as the concentration of homocysteine might be necessary to efficiently inhibit LDL oxidation by iron(III) and copper(II) in the presence of homocysteine and cystine. Histidine increased the efficiency of ascorbic acid as an antioxidant against copper-mediated oxidation in this system. The capacity of homocysteine to regenerate ascorbic acid from dehydroascorbic acid appeared to play a minor role in inhibition of ascorbic acid oxidation by copper as compared to copper chelation by homocysteine.     

Effects of dietary calcium on the metabolism of trace elements in male and female rats

The effect of dietary calcium on the metabolism of iron, zinc, copper, and manganese in male and female rats was investigated. For 3 or 6 weeks the rats were fed three diets containing: (1) 0.26, (2) 0.52, or (3) 2.08% Ca. The apparent absorption of iron was depressed by the high calcium diet, and manganese absorption was highest in the low calcium groups. Generally there was a decrease in the absorption of minerals from 3 to 6 weeks. With an increase in the dietary calcium the absorption of Ca and P decreased. The liver iron concentration in the females fed diet 3 decreased from about 600 to 200 microg/g dry weight. The high calcium intake also caused a slight increase in the heart calcium levels in both sexes. However, diet 3 prevented kidney calcification in the female rats at 6 weeks and this was attributed to a dramatic decrease in the urinary phosphorus, although the calcium had increased about 40 times. In males, on the other hand, the high calcium diet caused some kidney calcification.     

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.     

Dose-effect of dietary oleic acid: oleic acid is conditionally essential for some organs

The minimum dietary intake of oleic acid that is indispensable to maintain a normal content of this fatty acid in several tissues (heart, muscle, kidney and testis) was determined in the rat. For this purpose, a dose-effect study was conducted using an experimental protocol with 7 groups of rats who received a diet in which the oleic acid level varied from 0 to 6000 mg per 100 g diet, but the other ingredients were identical (in particular the essential fatty acids, linoleic and alpha-linolenic acid). Female rats were fed the diets from two weeks before mating, and their pups were killed aged either 21 or 60 days. When the level of oleic acid in the diet was increased, the main modifications observed in 21-day-old deficient pups were as follows: (i) for 18:1n-9, in the liver, muscle, heart, kidney, and testis, a plateau was reached at about 4 g oleic acid per 100 g diet. Below this level, the higher the dose the greater the response; (ii) for 16:1n-7, the concentration decreased in the liver, muscle, heart, kidney and testis; (iii) the concentration of 18:1n-7 decreased in the kidney, muscle, and testis; (iv) some minor modifications were noted for the other fatty acids. In mother's milk at 14 days of lactation, when dietary oleic acid increased, the levels of 18:1(n-9) also increased; the increase was regular and did not reach a plateau. In 60-day-old rats, the results were generally similar to those in 21-day-old rats, but with some differences, in particular a slight decrease in oleic acid concentration in the liver and kidney at the highest dietary oleic acid level.     

High dietary aluminum affects the response of rats to silicon deprivation

Antagonistic interactions between silicon and aluminum occur in living organisms. Thus, an experiment was performed to ascertain whether high dietary aluminum would accentuate the signs of silicon deprivation in rats and conversely whether silicon deprivation would accentuate the response to high dietary aluminum. The experiment was factorially arranged with two variables: silicon as sodium metasilicate, 0 or 40 μg/g diet, and aluminum as aluminum citrate, 0 or 500 μg/g diet. After 9 wk, body weights and plasma urea nitrogen were higher and plasma concentrations of threonine, serine, glycine, cystine, and methionine were lower in silicon-adequate than silicon-deprived rats. High dietary aluminum significantly decreased plasma phenylalanine. An interaction between aluminum and silicon affected plasma triglyceride, cholesterol, and phosphorus concentrations. High dietary aluminum decreased these variables when silicon was absent from the diet, but increased them when silicon was present. Skull iron and silicon concentrations were decreased and iron and zinc concentrations in the femur were increased by the addition of 500 μg Al/g diet. High dietary aluminum decreased tibia density in silicon-adequate rats, but increased tibial density in silicon-deprived rats. The findings indicate that in rats, high dietary aluminum can affect the response to silicon deprivation and dietary silicon can affect the response to high dietary aluminum.