Development of iron deficiency decreases zinc requirement of rats

Effects of the development of Fe deficiency on changes in Fe and Zn metabolism and its possible interactions with dietary Zn were determined. Adequate (25 microg/g) and marginally deficient (5 microg/g) Zn diets containing a sufficient (40 microg/g) dietary Fe levels were fed for 2 wk. Thereafter, both dietary Zn groups were fed an Fe-deficient (2.2 microg/g) diet for 4 wk. It was found that the effects of an Fe-deficient diet began to occur 7 and 14 d after feeding the Fe-deficient diet. At this time, tissue Fe concentrations were depleted and rats were unable to maintain hemoglobin levels. The Fe-deficient diet also induced an immediate fall in plasma Fe concentration, transferrin saturation, and apparent Fe absorption, while the concentrations of liver cytochrome c increased as Fe deficiency developed. Decreases in liver and spleen Fe levels, as well as the activities of blood and bone marrow aminolevulinic acid dehydratase (ALA-D, EC 4.2.1.24) were observed 3, 7, and 14 d after feeding the Fe-deficient diet, and thereafter they were increased. On the other hand, the activity of plasma alkaline phosphatase (ALK-P, EC 3.1.3.1) decreased continuously as Fe deficiency progressed. With severe development of Fe deficiency, rats fed the Zn-adequate diet had increased levels of Zn concentration in the plasma, liver, spleen, kidney, and femur, whereas apparent Zn absorption was decreased. The decrease in apparent Zn absorption and the increase in tissue Zn concentration of rats might be related to the lowered Zn requirement, which is associated with the depressed Zn metabolism caused by feeding Fe-deficient diets.     

Development of alimentary zinc deficiency in growing rats is retarded at low dietary protein levels

The aim of the present study was to determine whether the level of dietary protein would influence the onset of zinc deficiency in rats because zinc-deprived rats have problems metabolizing dietary protein. Young male Sprague-Dawley rats were fed isoenergetic Zn-deficient diets (0.8 mg Zn/kg diet) or control diets substituted with zinc sulfate (54 mg Zn/kg diet) and protein levels of 2, 5, 8, 10, 15, 20 or 25 g/100 g for 21 d to determine whether changing the protein level of Zn-deficient diets affects the Zn status of the rats. In rats fed low dietary protein levels of 2 and 5%, feed intake, growth and appearance did not differ between the Zn-deficient rats and the control rats because the low zinc requirement was met by mobilization of zinc from the skeleton. At higher dietary protein levels, the Zn-depleted rats developed marked signs of Zn deficiency and had reduced feed intake, growth, alkaline phosphatase activity in the serum and Zn concentrations in serum and femur compared with the control rats. The reduced feed intakes and decreased growth of Zn-depleted rats fed high dietary protein levels (20 and 25%) compared with control rats may be due to disturbed protein synthesis, as demonstrated by the increased activities of alanine aminotransferase, glutamate dehydrogenase and carbamoylphosphate synthetase in the liver. Zinc as an essential component of the diet is thus vital for the efficient utilization of dietary protein.     

Level of dietary iron,not type of dietary fat,is hyperlipidemic in copper-deficient rats

OBJECTIVE: This study was conducted to determine whether high dietary iron will negate the protective effect of unsaturated fat against hyperlipidemia. METHODS: Forty-eight weanling, male Sprague Dawley rats were randomly assigned to eight dietary groups differing in the levels of copper and iron and type of dietary fat (saturated or unsaturated). The diets were either deficient (0.6 microg Cu/g) or adequate (6.8 microg Cu/g) copper and either adequate (53 microg Fe/g) or high (506 microg Fe/g) iron. All diets contained starch as the sole source of dietary carbohydrate. RESULTS: Regardless of the type of dietary fat, three copper-deficient rats fed the high levels of dietary iron died prematurely due to ruptured hearts. Surviving rats belonging to the copper deficiency and high-dietary iron regimen developed severe anemia, enlarged hearts and livers, and exhibited the highest levels of liver iron. These rats also developed hypercholesterolemia. Triglycerides were elevated by the consumption of high iron diets. CONCLUSION: Data show that levels of dietary iron, not the type of dietary fat, are potential inducers of hypertriglyceridemia. Data also show that the combination of high iron intake and dietary copper deficiency is responsible for elevating blood cholesterol.     

The effect of different dietary levels of vitamin A on metabolism of copper iron and zinc in the chick

Chicks were fed on diets containing either no added vitamin A or 3300 micrograms/kg or 330,000 micrograms/kg retinol equivalents for 30 d. Concentrations of copper, iron and zinc were higher in liver and lower in plasma at low and high intakes of vitamin A. Haemoglobin, packed cell volume and erythrocyte levels were depressed by both low and high vitamin A intake and could be related to vitamin A levels by quadratic equations. The Zn and Fe levels in erythrocytes and serum albumin and ceruloplasmin were also affected in a similar fashion by low or high vitamin A diets. Hepatic activity of alcohol dehydrogenase (EC 1.1.1.1) and cytochrome oxidase (EC 1.9.3.1) paralleled Zn and Cu concentrations respectively. Superoxide dismutase (EC 1.15.1.1) and hydrolysis of triolein and retinyl palmitate were not correlated significantly with concentrations of metals but were correlated negatively with log vitamin A concentration. No changes in bone concentrations of Cu, Fe or Zn were detected. It is suggest that vitamin A influences metabolism of Cu, Fe and Zn possibly, in part, due to a decrease in secretion of transport proteins by the liver.     

Development of anemia in copper-deficient rats fed high levels of dietary iron and sucrose

The effects of dietary carbohydrate and iron on the development of copper deficiency were examined. Male Sprague-Dawley rats (n = 48) were limit-fed one of eight diets in a 2 X 2 X 2 factorial design for 19 d. Two levels of copper (0.85 or 8.6 micrograms Cu/g diet) and iron (54 or 226 micrograms Fe/g diet) and two types of carbohydrate (sucrose or cornstarch, 65.3%) were fed. Compared with control rats, copper-deficient rats had lower hematocrits, lower ceruloplasmin levels, lower tissue levels of copper and increased hepatic iron levels. Copper-deficient rats fed sucrose had significantly lower hematocrits, lower apparent absorption of copper, lower liver iron levels and higher plasma triglyceride levels than copper-deficient rats fed cornstarch. Copper-deficient rats fed sucrose with 226 micrograms Fe/g diet had hematocrit levels that were 15% lower than all other copper-deficient levels and 23% lower than control levels. Tissue levels of copper among copper-deficient rats were not affected by the type of carbohydrate or by the level of dietary iron. These data indicate that both high iron and sucrose can affect the development of the copper deficiency.     

Maternal zinc deficiency raises plasma prolactin levels in lactating rats

There is an inverse relation between zinc (Zn) intake and plasma prolactin in men and nonpregnant women. Whether a relation exists in lactating women is unknown, despite the potential consequences of perturbations in prolactin regulation on lactation performance. We examined the effects of low Zn intake on prolactin concentration, the prolactin regulatory pathway in the pituitary gland, and lactation performance in lactating rats. Female rats were fed diets containing 7 (zinc deficient; ZD), 10 (marginally zinc deficient; MZD) or 25 mg Zn/kg (control) from 70 d preconception to lactation d 11. Rats were killed, pituitary glands dissected, and tissues and plasma collected and analyzed for prolactin concentration. Pituitary gland pituitary factor 1 (Pit-1), dopamine 2 receptor (D2R), and prolactin receptor mRNA expression were measured in the pituitary gland. Liver, mammary gland, plasma, and milk Zn were measured. Milk intake of the pups was also recorded. Plasma prolactin concentration was higher in rats fed the ZD (125.9 microg/L) diet compared with control rats (21.7 microg/L). Pituitary gland prolactin concentration was higher in rats fed the ZD diet (69.8 mg/g total protein) compared with controls (29.0 mg/g). Plasma Zn concentration was lower in rats fed the MZD and ZD diets, and mammary gland and milk Zn concentrations were lower in rats fed the ZD diet compared with control rats. Rats fed the ZD diet had lower D2R, prolactin receptor, and Pit-1 mRNA levels, whereas rats fed the MZD diet had lower prolactin receptor and Pit-1 mRNA levels compared with control rats. Milk intake was lower in pups of rats fed the MZD and ZD diets. Our results suggest that marginal Zn nutriture may compromise milk production despite increased prolactin levels. In addition, increased circulating prolactin concentration is not due to altered nursing behavior, but may be due to alterations in the prolactin regulatory pathway in the pituitary gland.     

Iron, zinc and copper interactions: chronic versus acute responses of rats

Several methodologies were evaluated to study iron, zinc and copper interactions. In three studies, rats were fed diets containing adequate levels of iron (33-35 micrograms Fe/g diet) and zinc (15-25 micrograms Zn/g diet) and diets with excessive levels of zinc (2441-2470 micrograms Zn/g diet) or iron (1408-3042 micrograms Fe/g diet). Consumption of excess iron for several weeks or in one test meal did not alter tissue levels of zinc or apparent absorption of 65Zn. In contrast rats fed excess zinc throughout the three studies had depressed hematocrits and serum copper levels, apparently absorbed 59Fe less efficiently and retained less 59Fe in livers and tibias than control animals. Nutritional status with regard to iron or zinc, not just the intakes of iron and zinc, also influenced the interactions between zinc and iron. Rats fed excess iron for several weeks retained less 65Zn from a test meal in their tibias than rats fed excessive iron in only the test meal. Although chronic ingestion of excess zinc depressed apparent absorption of 59Fe from a test meal, the ingestion of one test meal with excess zinc did not. Investigators studying nutrient interactions should not rely solely on studies in which unadjusted humans or animals are given a single dose of test substances because acute responses do not reflect all the changes induced by chronic feeding.     

Mineral status of female rats affects the absorption and organ distribution of dietary cadmium derived from edible sunflower kernels (Helianthus annuus L.)

The intake of food cadmium (Cd) in microg/day over time can increase the body burden of this element. Some human populations that consume subsistence rice-based diets low in calcium (Ca), iron (Fe), and zinc (Zn) are more susceptible to Cd poisoning than populations that consume more nutritious diets. This study determined the effects of marginal deficiencies of these essential elements on the absorption and organ retention of Cd from a natural food that contains Cd, edible sunflower kernels (Helianthus annuus L.; SFK). Weanling female rats were fed diets containing 20% SFK in a 2x2x2 factorial design with marginal and adequate amounts of Ca, Zn, and Fe. Marginal Zn (11 mg/kg) and Fe (13 mg/kg), and Cd (0.18 mg/kg) were derived solely from 20% SFK. These amounts of Fe and Zn represented 39 and 90% of the NRC requirement for the rat, respectively. The marginal dietary Ca concentration (2.5 g/kg) was one-half the NRC requirement. After 5 weeks on the experiment, rats were fed 1 g of their respective diets containing SFK extrinsically labeled with 37 kBq 109Cd, and absorption was determined by whole-body counting techniques. Rats were then killed and organs collected for 109Cd assays. No effect of treatment on weight gain was observed; however, when dietary Zn was low, feeding marginal Ca elevated Cd absorption by 50% (P<0.05) over those fed adequate Ca and Zn. Feeding marginal Fe elevated Cd absorption >2.5-fold (P<0.001) over those fed adequate Fe. In contrast, the naturally occurring Zn in SFK that provided 90% of the rat's requirement was enough to deter excessive absorption of Cd and enough to alone prevent significant elevation of organ Cd. Organ content of 109Cd and Cd followed the same general pattern as whole-body absorption. These data show that marginal nutritional deficiencies of Ca and Fe can readily enhance the body burden of Cd that comes from the diet. Also, some natural competitors of Cd, such as Zn, contained in foods can independently minimize Cd absorption.     

The effect of combined dietary iron, calcium and folic acid supplementation on apparent 65Zn absorption and zinc status in pregnant rats

In the present study the effect of combined iron, calcium and folic acid supplementation of the diet on 65Zn retention and zinc status was studied in the pregnant rat. Female Wistar rats were fed on a low- (8 micrograms/g) or high- (60 micrograms/g) Zn diet for 14 d and then mated overnight. After mating, half the rats were fed on the low- or high-Zn diet as before, whilst the other half were fed on similar diets supplemented with Fe, Ca and folic acid. The level of supplementation was chosen to reflect proportionately the possible increase in daily intakes of these nutrients by pregnant women. Rats which did not mate successfully were used as non-pregnant controls. On day 18 of pregnancy, each animal was given a meal of the appropriate diet labelled extrinsically with 65Zn, and on day 20 rats were killed. Carcass 65Zn retention was lower in pregnant and non-pregnant rats fed on the supplemented diets compared with those fed on the unsupplemented diets. Rats which consumed the supplemented diets throughout pregnancy had reduced plasma Zn concentrations but femur and fetal Zn concentrations were unaffected. Maternal femur Ca and fetal Fe concentrations were lower in the high-Zn groups compared with rats fed on low-Zn diets. It was concluded that the risk of inducing fetal Zn depletion as a consequence of Fe, Ca and folic acid supplementation during pregnancy appeared to be slight.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of varying dietary zinc levels on the concentration and localization of zinc in rat bile-pancreatic fluid

To determine if zinc homeostasis occurs by zinc output from bile-pancreatic secretions, the bile-pancreatic duct and intestine of rats were surgically cannulated, and bile-pancreatic fluid was collected 2 h/d from the day of surgery to 8 d after surgery. The rats were fed diets containing 10, 100 or 1000 micrograms Zn/g diet before and after surgery. The effect of surgery itself was significant; food intake was initially lower than presurgery levels, but returned to presurgery levels by d 5. Protein and zinc concentrations, and carboxypeptidase A (CpA) and carboxypeptidase B (CpB) activities in bile-pancreatic fluid increased after surgery and leveled off at approximately d 6. Among the dietary zinc groups, the concentration of zinc in bile-pancreatic fluid varied significantly, whereas concentrations of calcium and copper did not. Zinc concentration in bile-pancreatic fluid for d 1-8 postsurgery averaged 1.8, 3.2 and 4.4 micrograms Zn/g, in the groups fed 10, 100 and 1000 micrograms Zn/g diet, respectively. Because the percent of zinc ingested that was secreted in bile-pancreatic fluid, estimated to be 57, 9.5 and 1.2% for the groups consuming the diets containing 10, 100 and 1000 micrograms Zn/g diet respectively, was not similar in the three groups, the quantity of zinc in bile-pancreatic fluid is not proportionally related to the amount of zinc ingested. Our results therefore suggest that zinc secretion in bile-pancreatic fluid does not play a major role in zinc homeostasis. Molecular localization of zinc in bile-pancreatic fluid and measurement of activity of CpA and CpB indicated that zinc in bile-pancreatic fluid is associated primarily with these digestive enzymes.     

Excess dietary zinc decreases tissue alpha-tocopherol in chicks

Experiments were conducted to determine the basis of the reduction in tissue alpha-tocopherol concentrations by excess dietary zinc (Zn) in chicks fed purified diets. These reductions were preceded by elevations in the Zn concentrations of plasma and pancreas, and in the amylase activity of plasma and by reductions of exportable enzymes of the pancreas. Chicks fed similar levels of Zn as supplements to a non-purified diet showed no such impairments in either exocrine pancreatic function or tissue alpha-tocopherol concentrations. Depression of feed intake and subsequent changes of concentrations of tissue lipid components by excess dietary Zn accounted for only a minor portion of the reduction of tissue alpha-tocopherol concentrations. Tissue alpha-tocopherol concentrations were moderately correlated with tissue lipid concentrations. The rate of appearance of radioactivity from an oral dose of all-rac-alpha-tocopherol-[3,4-3H]2 in plasma was reduced by 64% by addition of 500 mg Zn/kg to the purified diet for 2 wk. These results indicate that impaired enteric absorption and/or transport of vitamin E as a consequence of Zn-induced pancreatic insufficiency is a major cause of reduced tissue concentrations of alpha-tocopherol produced by excess dietary Zn.     

Behavioral and hematologic consequences of marginal iron-zinc nutrition in adolescent monkeys and the effect of a powdered beef supplement

BACKGROUND: The adolescent growth spurt and menarche increase iron and zinc needs and could precipitate functional deficiencies if dietary sources are inadequate. OBJECTIVE: The effects of mild, combined zinc and iron deprivation during the growth spurt and the ability of meat as a common dietary source of zinc and iron to reverse these effects was studied. DESIGN: Pubertal female rhesus monkeys were fed control diets (n = 8) or diets marginally deficient in zinc (2 microg/g diet; n = 8) and iron (10 microg/g diet; n = 8) for 3 mo. A powdered beef supplement (104 microg Zn/g and 43 microg Fe/g, 11 +/- 2 g/d) was then fed daily to half of the deprived group for 3 additional months. RESULTS: Growth and hematology were not affected significantly by iron-zinc deprivation, but plasma zinc and iron were somewhat lower in the deprived group than in the control group after 3 mo. The deprived monkeys reduced their participation in behavioral testing, responded more slowly and less frequently to test stimuli, and were less active. The beef supplement increased participation in testing and stabilized activity levels, but response times remained depressed. Plasma ferritin was lower in the nonsupplemented deprived monkeys than in the controls by the end of the experiment. Four of 8 of the deprived monkeys had iron deficiency anemia compared with none of the controls and 1 of 8 who received the beef supplement. CONCLUSIONS: Marginal zinc and iron deprivation in early adolescence can lead to behavioral and hematologic dysfunction in nonhuman primates and dietary beef supplements can prevent and reverse some of these effects.     

Effect of varying dietary zinc intake of weanling mouse pups during recovery from early undernutrition on growth, body composition and composition of gain

Catch-up growth during recovery from undernutrition is characterized by rapid body weight gain often marked by disproportionately high fat gain. In this study dietary zinc intake of mouse pups during recovery from undernutrition affected composition of gain as well as growth. Mouse pups were undernourished during the suckling period and then fed 25% casein recovery diets containing 5, 10, 40 or 110 micrograms Zn/g diet. Pups given dietary zinc levels of 40 micrograms Zn/g ad libitum achieved recovery body weights and had normal body composition. However, previously undernourished pups given marginal levels of dietary zinc (10 micrograms Zn/g diet) had similar food intakes, similar final body weights, lower lean body mass gains and greater fat gains (males only) than controls. Pups fed low zinc diets (5 micrograms Zn/g diet) were unable to attain recovery body weight and had less protein gain than previously undernourished animals fed higher zinc-containing diets or healthy pups fed the same zinc levels. The results were consistently more pronounced in males. Thus dietary zinc deficiency during catch-up growth after undernutrition limited both recovery and protein gain, whereas marginal dietary zinc intake limited protein gain in mice.     

Influence of dietary lipids on iron and copper levels of rats administered oral contraceptives.

Interrelationships between oral contraceptives and dietary lipids on iron and copper levels in plasma and tissues were investigated in rats. Diets containing either 20% (by weight) safflower oil or hydrogenated coconut oil with and without cholesterol (0.5%) were fed to weanling, female, Wistar-strain rats for a period of 19 weeks. Three types of oral contraceptive agents differing in estrogen/progesterone ratios were administered during weeks 16 through 19 of the experiment. Control rats received the dietary treatment without oral contraceptives. Hemoglobin concentration, hematocrit, red blood cell counts, mean cell hemoglobin and hemoglobin concentration, and mean cell volume values were similar among the various dietary and drug-treatment groups. Elevated levels of copper were found in livers of drug-treated animals fed diets containing cholesterol and safflower oil, whereas levels of copper or iron in spleen and kidney were not influenced by oral contraceptives. Dietary safflower or coconut oil had no influence on levels of iron or copper in plasma. However, iron levels were higher in liver, spleen, and kidneys of rats fed coconut oil compared with those fed safflower oil. Cholesterol-fed rats had reduced levels of iron in plasma and tissues and increased levels of copper in plasma and liver. Iron deficiency in cholesterol-fed rats was indicated by low levels of iron in plasma, liver, spleen, and kidney. In experiment 2, animals were fed the 20% safflower oil diet, with and without sodium glycocholate or cholesterol, to determine whether the apparent malabsorption of iron resulted from sodium glycocholate or cholesterol. Sodium glycocholate resulted in a marked increase in the absorption of iron, whereas cholesterol depressed absorption.     

Dietary cellulose, zinc and copper: effects on tissue levels of trace minerals in the rat.

This study was designed to examine the effect of graded levels of cellulose, zinc and copper on tissue mineral levels. Tissue mineral levels were assayed by atomic absorption spectrophotometry in samples collected from a study which involved 12 treatments in a 3 X 2 X 2 factorial arrangement. This study involved three levels of cellulose (0, 8, and 16% of the diet), two levels of Cu (deficient and adequate; 2 and 18 mg/kg of diet, respectively), and two levels of Zn (marginal and abundant; 10 and 120 mg/kg of diet, respectively). Six weanling, male Sprague-Dawley rats were assigned to each treatment and after 9 weeks they were killed. Reductions of tissue Cu content were observed in the serum, liver, tibia and testis of the rats fed the Cu-deficient diets. The Fe content of the tibia and testis was reduced, but that of liver was elevated in the rats fed Cu-deficient diets. Reductions in tibial Zn levels were observed in the rats fed marginal-Zn as compared to those fed the abundant-Zn diets; and in the rats fed Cu-adequate as compared to those fed Cu-deficient diets. Increases in cellulose resulted in increased liver and testicular Cu content only in rats fed the Cu-deficient diets. Additions of cellulose appeared to have no adverse effect on the distribution of Zn, Cu and Fe in tissues which are sensitive to dietary deficiencies. With the exception of rats fed the copper-deficient, marginal zinc diets, the rats fed the other diets demonstrated a small reduction in serum zinc values as cellulose was increased.     

Copper, iron, zinc, and selenium dietary intake and status of Nepalese lactating women and their breast-fed infants

The dietary intake of copper, iron, zinc, and selenium of 26 Nepalese lactating mothers was estimated from chemical analysis of 24-h food and beverage composites. Fasting blood and milk samples were obtained from the mothers and blood samples were obtained from the infants. The Nepalese mothers consumed significantly more Cu, significantly less Fe and Se, and similar amounts of Zn as compared with American lactating women. Blood Fe status indices and plasma concentrations of Cu, Zn, and Se were lower in the Nepalese mothers than in the American mothers. These lower values may in part be related to the high neutral detergent fiber and phytate content of the Nepalese diet, which could make these minerals less available for absorption. The high exposure to infections in Nepal may also depress Fe status indices and plasma Zn concentrations. The lower dietary Se intake of the Nepalese mothers was reflected in lower milk concentrations.     

Dietary copper primarily affects antioxidant capacity and dietary iron mainly affects iron status in a surface response study of female rats fed varying concentrations of iron, zinc and copper.

This study was designed to examine the interactions among dietary iron (Fe), copper (Cu), and zinc (Zn) and their effects on Fe status and oxidative stress in female rats. In a three-factor central composite response surface design, rats were assigned to 15 groups and fed modified AIN-93G basal diets with varying amounts of Fe and Zn (7.0, 15.5, 45.8, 135.6, or 300 micrograms/g diet) and Cu (0.5, 1.1, 3.2, 9.2, or 20 micrograms/g diet) for 6 wk. Variations in hemoglobin, hematocrit, and serum ferritin were mainly related to dietary Fe. Liver nonheme Fe was directly affected by dietary Fe and was slightly attenuated by interactions between Cu and Zn, and Zn and Fe. Serum ceruloplasmin activity was primarily determined by an interaction between Cu and Zn with substantial moderation by the quadratic effect of dietary Cu. Liver and heart total superoxide dismutase (SOD) and Cu/Zn SOD activities were directly affected by dietary Cu. Dietary Fe was the only significant, yet weak, predictor of liver thiobarbituric acid reactive substances (TBARS) and vitamin E content and serum triacylglycerols. Variability in serum Cu was mostly determined by the interaction between Cu and Fe, with modification from the quadratic effect of dietary Cu. Serum Zn varied with dietary Zn with a small negative influence from the interaction between Cu and Fe. In summary, Fe status was minimally influenced by dietary Zn or Cu, and Fe intakes 10-fold greater than required did not induce overt oxidative stress in female rats. In addition, measures of antioxidant capacity were primarily influenced by dietary Cu and were optimal at moderate intakes of this micronutrient.     

Varying levels of manganese and iron affect absorption and gut endogenous losses of manganese by rats.

The interactive effects of manganese and iron on true absorption and endogenous losses of manganese were investigated by feeding rats three levels of manganese (0.9, 48 or 188 micrograms Mn/g diet) and two levels of iron (19 or 276 micrograms Fe/g diet) for 7 wk. After 45 d, half of the rats were fed 54Mn and half were injected intraportally with 54Mn complexed to albumin. The relative distribution of 54Mn in tissues was generally similar for rats when 54Mn was administered in these two ways. Manganese-deficient animals retained more of the isotope, had both higher apparent and higher true absorption of manganese, had a greater proportion of 54Mn in their livers and had a lower proportion of 54Mn in their muscles compared with animals fed adequate or high levels of manganese. High iron intake inhibited manganese true absorption, reduced tissue manganese concentrations and inhibited heart manganese-dependent superoxide dismutase activity. However, the greatest effect of dietary iron was on mucosal cell manganese concentrations. Endogenous losses of manganese were approximately 8% of the amount of manganese actually absorbed regardless of intake. Thus, control of absorption in the gut seems to be the major way that manganese homeostasis is maintained. Furthermore, iron seems to be depressing manganese absorption by inhibiting manganese uptake into the mucosal cells.     

Tin, copper, iron and calcium metabolism of rats fed various dietary levels of inorganic tin and zinc

Three studies were conducted to determine the effects of various dietary levels of tin (less than 1, approximately 100, approximately 200, approximately 500, approximately 2000 micrograms/g diet) and of zinc (approximately 15, approximately 30, approximately 52 micrograms/g diet) on the metabolism of tin, copper, iron and calcium by growing rats. The accumulation of tin in the kidneys and tibias of animals was proportional to dietary exposure. The concentration of tin in the bones of rats fed greater than 100 micrograms Sn/g diet was 5-fold and 20-fold greater than the levels found in kidney and liver, respectively. Rats fed greater than 500 micrograms Sn/g diet had plasma copper levels that were only 13% of control levels and had depressed copper levels in livers and kidneys. The activity of delta-aminolevulinic acid dehydratase in the erythrocytes of rats fed the highest level of tin was 55% of that found in control animals. The amounts, but not the concentrations, of calcium in the tibias of rats fed greater than 100 micrograms Sn/g diet were less than the levels in the bones of control animals. The moderate variations in dietary zinc levels did not affect significantly the levels of minerals in tissues.     

Influences of dietary protein levels and phytate contents on zinc requirement in rats

This study investigates whether the effects of increased dietary levels of soy protein on zinc-deficient rats are due to the dietary protein content. Rats were fed two levels of demineralized soy protein (DP) diets and two levels of egg albumin (EA) diets including 7 ppm zinc (Experiment 1). Growth was depressed in rats fed a 20% DP diet (0.43% phytate) but not in those fed a 10% EA diet containing 7 ppm zinc. Zinc concentrations in the serum, femur and kidney were lower in rats fed the 20% DP diet than those fed a 10% DP (0.20% phytate) diet, and they were also lower in rats fed the 10% EA diet than those fed a 5% EA diet. Zinc concentrations in the serum and femur of rats fed the 10% DP diet or the 20% DP diet were decreased compared with those fed the 5% EA diet or the 10% EA diet, respectively. Under zinc-deficient conditions (<0.4 ppm Zn), the survival time shortened (Experiment 2) and the zinc concentration in the serum and femur decreased faster (Experiment 3) in rats fed the 10% EA diet compared with those fed the 5% EA diet. The survival times and time courses of these parameters show that the zinc requirements of rats increased with the dietary protein level. The increased zinc requirement of rats that accompanied increasing dietary soy protein was due to the dietary protein content as well as the dietary phytate content.