Carol D. Seaborn

University of Wisconsin - Stout, Menominee, Wisconsin, United States

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Publications (21)36.96 Total impact

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    C D Seaborn, F H Nielsen
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    ABSTRACT: Both arginine and silicon affect collagen formation and bone mineralization. Thus, an experiment was designed to determine if dietary arginine would alter the effect of dietary silicon on bone mineralization and vice versa. Male weanling Sprague-Dawley rats were assigned to groups of 12 in a 2 x 2 factorially arranged experiment. Supplemented to a ground corn/casein basal diet containing 2.3 microg Si/g and adequate arginine were silicon as sodium metasilicate at 0 or 35 microg/g diet and arginine at 0 or 5 mg/g diet. The rats were fed ad libitum deionized water and their respective diets for 8 wk. Body weight, liver weight/body weight ratio, and plasma silicon were decreased, and plasma alkaline phosphatase activity was increased by silicon deprivation. Silicon deprivation also decreased femoral calcium, copper, potassium, and zinc concentrations, but increased the femoral manganese concentration. Arginine supplementation decreased femoral molybdenum concentration but increased the femoral manganese concentration. Vertebral concentrations of phosphorus, sodium, potassium, copper, manganese, and zinc were decreased by silicon deprivation. Arginine supplementation increased vertebral concentrations of sodium, potassium, manganese, zinc, and iron. The arginine effects were more marked in the silicon-deprived animals, especially in the vertebra. Germanium concentrations of the femur and vertebra were affected by an interaction between silicon and arginine; the concentrations were decreased by silicon deprivation in those animals not fed supplemental arginine. The change in germanium is consistent with a previous finding by us suggesting that this element may be physiologically important, especially as related to bone DNA concentrations. The femoral and vertebral mineral findings support the contention that silicon has a physiological role in bone formation and that arginine intake can affect that role.
    Biological Trace Element Research 01/2003; 89(3):239-50. DOI:10.1385/BTER:89:3:239 · 1.61 Impact Factor
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    C D Seaborn, F H Nielsen
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    ABSTRACT: We have shown that silicon (Si) deprivation decreases the collagen concentration in bone of 9-wk-old rats. Finding that Si deprivation also affects collagen at different stages in bone development, collagen-forming enzymes, or collagen deposition in other tissues would have implications that Si is important for both wound healing and bone formation. Therefore, 42 rats in experiment 1 and 24 rats in experiment 2 were fed a basal diet containing 2 or 2.6 microg Si/g, respectively, based on ground corn and casein, and supplemented with either 0 or 10 microg Si/g as sodium metasilicate. At 3 wk, the femur was removed from 18 of the 42 rats in experiment 1 for hydroxyproline analysis. A polyvinyl sponge was implanted beneath the skin of the upper back of each of the 24 remaining rats. Sixteen hours before termination and 2 wk after the sponge had been implanted, each rat was given an oral dose of 14C-proline (1.8 microCi/100 g body wt). The total amount of hydroxyproline was significantly lower in the tibia and sponges taken from Si-deficient animals than Si-supplemented rats. The disintegrations per minute of 14C-proline were significantly higher in sponge extracts from Si- deficient rats than Si-supplemented rats. Additional evidence of aberrations in proline metabolism with Si deprivation was that liver ornithine aminotransferase was significantly decreased in Si-deprived animals in experiment 2. Findings of an increased accumulation of 14C-proline and decreased total hydroxyproline in implanted sponges and decreased activity of a key enzyme in proline synthesis (liver ornithine aminotransferase) in Si-deprived animals indicates an aberration in the formation of collagen from proline in sites other than bone that is corrected by Si. This suggests that Si is a nutrient of concern in wound healing as well as bone formation.
    Biological Trace Element Research 01/2003; 89(3):251-61. DOI:10.1385/BTER:89:3:251 · 1.61 Impact Factor
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    ABSTRACT: Sporadic reports have appeared that suggest silicon plays a functional role in immune function by affecting lymphocyte proliferation. In addition, there is also considerable interest in supplemental arginine as a modulator of immune function. Therefore, the purpose of this animal experiment was to determine the effect of supplemental compared to adequate arginine on immune function as measured by splenic T-lymphocyte proliferation in the presence of adequate or inadequate dietary silicon. The independent variables were, per gram of fresh diet, silicon supplements of 0 or 35 microg and arginine supplements of 0 or 5 mg. The basal diet contained 2.3 microg silicon/g and 7.82 mg L-arginine/g. After feeding the male rats (nine per treatment group) for 8 wk, spleen lymphoid cells were isolated and cultured with methyl-3[H]thymidine. Supplemental arginine significantly decreased Con-A-induced DNA synthesis of splenic T-lymphocytes, but the response to arginine was influenced by dietary silicon. The decreased DNA synthesis was more marked when rats were fed adequate silicon than when fed inadequate silicon. Also, when arginine was not supplemented, DNA synthesis was higher in lymphocytes from rats fed an adequate silicon diet than rats fed the inadequate silicon diet. These findings support the huypothesis that an interaction between silicon and arginine affects immune function and that inadequate dietary silicon impairs splenic lymphocyte proliferation in response to an immune challenge.
    Biological Trace Element Research 02/2002; 87(1-3):133-42. DOI:10.1385/BTER:87:1-3:133 · 1.61 Impact Factor
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    C.D. Seaborn, F.H. Nielsen
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    ABSTRACT: Because arginine has been established as an essential amino acid for collagen formation, and several bone-remodeling proteins are rich in cysteine, we performed a study to ascertain whether supplemental arginine (Arg) and cystine (Cys) would affect bone collagen and mineral composition changes in animals deprived of silicon (Si). Male weanling Sprague-Dawley rats were randomly assigned to treatment groups of 12 in a 2 × 2 factorially arranged experiment. The rats were fed for 9 weeks a basal casein–ground corn–corn oil diet containing per g 2 μg Si, 1.7 mg Cys, 4.7 mg methionine, and 7.8 mg Arg. The independent treatment variables, per g fresh diet, were supplemental Si (as sodium metasilicate) at 0 and 35 μg and Cys or Arg at 0 and 12 mg. Silicon deprivation decreased the concentration of hydroxyproline in femur and potassium in vertebra. An interaction between Si and amino acid supplementation affected hematocrit, liver iron concentration, and bone copper and manganese concentrations. In animals deprived of Si, Cys supplementation compared to Arg supplementation depressed hematocrit, liver iron concentration, and tibia and vertebral copper concentrations and increased tibia and vertebral manganese concentrations. On the other hand, in animals fed adequate Si, supplemental Cys compared to supplemental Arg increased hematocrit, liver iron concentration, and tibia and vertebral copper concentrations and decreased tibia and vertebral manganese concentrations. Dietary Si also influenced the effect of Cys on mineral composition of the vertebra. The calcium and phosphorus concentrations in the vertebra were markedly increased by supplemental Cys compared to supplemental Arg when dietary Si was inadequate but had no effect on these concentrations when dietary Si was adequate. These findings indicate that silicon is needed for collagen formation, that high dietary Cys enhances changes induced by Si deprivation in trabecular-rich bone, and that Si nutriture has more impact on trabecular-rich bone than in cortical-rich bone. J. Trace Elem. Exp. Med. 15:113–122, 2002. Published 2002 Wiley-Liss, Inc.
    The Journal of Trace Elements in Experimental Medicine 01/2002; 15(3):113 - 122. DOI:10.1002/jtra.10011
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    ABSTRACT: Effects of five over-the-counter drugs on retention and urinary excretion of 51chromium from 51chromium chloride (51CrCl3) were evaluated using adult female rats. In addition to the control group dosed with distilled water (pH 7.89), groups were dosed with vitamin C (5 mg, pH 2.76), Tums® (40 mg, pH 9.72), Maalox Plus® (40 mg, pH 8.39), aspirin (40 mg, pH 2.74) or Bufferin® (40 mg, pH 8.73). After a 12 h fast, the drugs were administered by gastric intubation (0.5 ml) followed immediately by an oral dose of 51CrCl3 (55 uCi) in 0.14 M HCl (50 ul). Blood was sampled from the tail at 0.75, 1.5, 3.0 and 6.0 h. Urine samples were composited at 3, 6, and I2 h and tissues were sampled at 12 h. 51Chromium in blood, urine and tissues was higher (p<0.0001) in the aspirin group than in all other groups. The group dosed with Maalox had lower (p<0.0001) 51Cr in blood, urine and tissues than the other groups. Increased 51Cr absorption in the aspirin group and decreased 51Cr absorption in the Maalox group did not appear to be mediated solely by pH. Potential effects of long-term use of aspirin or antacids on Cr status need evaluation because over-the-counter drugs altered Cr absorption in this study.
    Nutrition Research 02/1995; 15(2-15):201-210. DOI:10.1016/0271-5317(95)92586-9 · 2.59 Impact Factor
  • M.L. Davis, C.D. Seaborn, B.J. Stoecker
    Nutrition Research 01/1995; 15(2). · 2.59 Impact Factor
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    Carol D. Seaborn, Forrest H. Nielsen
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    ABSTRACT: 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 x 4 factorially arranged experiment. The independent variables were, per gram fresh diet, Si (as sodium metasilicate) at 0 or 25 micrograms and Ge (as sodium germanate) at 0, 5, 30, or 60 micrograms. 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 evoked by Si supplementation. Additionally, some findings suggested that 60 micrograms 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 micrograms Ge/g diet had increased tibial DNA compared to animals fed 0 or 60 micrograms Ge; however, tibial DNA of animals fed 30 micrograms Ge was not statistically different from those animals fed 5 micrograms Ge. Thus, Ge may be of nutritional importance.
    Biological Trace Element Research 09/1994; 42(2):151-64. DOI:10.1007/BF02785386 · 1.61 Impact Factor
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    ABSTRACT: 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 and 14C distribution and excretion after a 14C 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 micrograms Cr/g diet, -Cr) or a Cr-adequate (2 micrograms 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 microCi of L-[carboxyl-14C] ascorbic acid and placed in metabolic cages. Ascorbate supplementation increased Fe concentrations in most analyzed tissues, hepatic 14C, 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, brain 14C and the amount of 14C expired as carbon dioxide. These findings suggest that dietary Cr may affect ascorbic acid metabolism and the metabolic response to stress.
    Biological Trace Element Research 07/1994; 41(3):279-94. DOI:10.1007/BF02917429 · 1.61 Impact Factor
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    Carol D. Seaborn, Forrest H. Nielsen
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    ABSTRACT: 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 micrograms/g diet, and aluminum as aluminum citrate, 0 or 500 micrograms/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 micrograms 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.
    Biological Trace Element Research 07/1994; 41(3):295-304. DOI:10.1007/BF02917430 · 1.61 Impact Factor
  • Carol D. Seaborn, Forrest H. Nielsen
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    ABSTRACT: Because boron resembles silicon in its chemical properties, an experiment was performed to determine if excessive dietary boron would affect the response to silicon deprivation and, conversely, if silicon would influence the effects of an excessive intake of boron. Male weanling Sprague-Dawley rats were assigned to groups of six or 12 in a two-by-two factorially arranged experiment. Supplemented to a ground corn/casein diet containing 1.2 μg silicon and 3 μg boron per gram were silicon as sodium metasilicate at 0 or 50 μg/g and boron as orthoboric acid at 0 or 500 μg/g diet. At nine weeks, animals fed high dietary boron had significantly decreased final body weights, liver-weight-to-body-weight ratios, urinary cAMP concentrations, plasma triglyceride, cholesterol, glycine, valine, leucine, and lysine concentrations and skull copper, sodium, and manganese concentrations. High dietary boron also significantly increased brain-weight-to-body-weight ratios, magnesium concentrations of femur, brain, and plasma, zinc concentration of femur, and iron concentration of skull. The bone mineral findings suggest that excess dietary boron exerts subtle effects on bone composition. Dietary silicon affected blood urea nitrogen, hematocrit, hemoglobin, and the concentrations of plasma threonine and aspartic acid in animals fed excess boron. Depression of the testes-weight-to-body-weight ratio of animals fed 500 μg boron per gram diet was most marked in animals not fed silicon. Although excessive dietary boron did not markedly enhance the response of rats to silicon deprivation, dietary silicon affected their response to high dietary boron. Thus, dietary silicon apparently can influence boron toxicity.
    Environmental Toxicology and Chemistry 06/1994; 13(6). DOI:10.1002/etc.5620130613 · 2.83 Impact Factor
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    C.D. Seaborn, F.H. Nielsen
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    ABSTRACT: Because boron resembles silicon in its chemical properties, an experiment was performed to determine if excessive dietary boron would affect the response to silicon deprivation and, conversely, if silicon would influence the effects of an excessive intake of boron. Male weanling Sprague-Dawley rats were assigned to groups of 6 or 12 in a two-by-two factorially arranged experiment. Supplemented to a ground corn/casein diet containing 1.2 [mu]g silicon and 3 [mu]g boron per gram were silicon as sodium metasilicate at 0 or 50 [mu]g/g and boron as orthoboric acid at 0 or 500 [mu]g/g diet. At nine weeks, animals fed high dietary boron had significantly decreased final body weights, liver-weight-to-body-weight ratios, urinary cAMP concentrations, plasma triglyceride, cholesterol, glycine, valine, leucine, and lysine concentrations and skull copper, sodium, and manganese concentrations. High dietary boron also significantly increased brain-weight-to-body-weight ratios, magnesium concentrations of femur, brain, and plasma, zinc concentration of femur, and iron concentration of skull. The bone mineral findings suggest that excess dietary boron exerts subtle effects on bone composition. Dietary silicon affected blood urea nitrogen, hematocrit, hemoglobin, and the concentrations of plasma threonine and aspartic acid in animals fed excess boron. Depression of the testes-weight-to-body-weight ratio of animals fed 500 [mu]g boron per gram diet was most marked in animals not fed silicon. Although excessive dietary boron did not markedly enhanced the response of rats to silicon deprivation, dietary silicon affected their response to high dietary boron. Thus, dietary silicon apparently can influence boron toxicity.
    Environmental Toxicology and Chemistry 06/1994; · 2.83 Impact Factor
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    Carol D. Seaborn, Shiang P. Yang
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    ABSTRACT: Molybdenum (Mo) supplementation reduces the incidence of nitrosamine-induced tumors in the esophagus and forestomach of laboratory animals, and the incidence of mammary cancer in female rats induced by N-nitroso-N-methylurea (NMU). The present study was conducted to evaluate the effect of graded amounts of Mo on NMU-induced mammary carcinogenesis, and on the excretion of Mo and copper (Cu). Female Sprague-Dawley rats aged 5 wk were given ad libitum a low-Mo (0.026 mg/kg) diet and deionized water. After 15 d, a single SC injection of 50 mg NMU/kg body wt was administered to each of 30 rats in groups 2-5. Eight rats in group 1 served as untreated control. One week after the carcinogen treatment, 0.1, 1.0, or 10 mg Mo from sodium molybdate were added to each liter of drinking water for groups 3, 4, and 5, respectively. Groups 1 and 2 did not receive any Mo supplementation. After the rats had been Mo-supplemented for 38, 67, and 85 d, 48-h urine and fecal samples were collected from the same 48 rats, and Mo and Cu were determined. Molybdenum seemed to have little effect on Cu excretion. At each time interval, animals fed 0 or 0.1 mg Mo/L excreted more Mo in feces than in urine, whereas rats fed 1 and 10 mg Mo/L water excreted more Mo in urine than in feces, which indicates that Mo absorption was not easily saturated as the amount of Mo increased. However, the liver became saturated with Mo when 0.1-1 mg Mo/L was fed. The total number of palpable tumors per group 101 d after NMU administration was 109, 115, 101, and 81, and the total carcinomas per group were 92, 96, 86, and 65 for the animals in groups 2-5, respectively. The results indicate that supplemental Mo in the amount of 10 mg/L of drinking water inhibited mammary carcinogenesis.
    Biological Trace Element Research 10/1993; 39(2-3):245-56. DOI:10.1007/BF02783194 · 1.61 Impact Factor
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    C D Seaborn, F H Nielsen
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    ABSTRACT: Ample evidence exists to indicate that silicon is essential for forming or maintaining normal healthy bones, brains and blood vessels, and thus may be a factor in the occurrence of some human diseases involving these tissues.
  • Carol D. Seaborn, Barbara J. Stoecker
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    ABSTRACT: Chromium and ascorbate depletion effects on 51chromium retention and excretion after a dose of 51CrCl3 were investigated in guinea pigs. Weanling animals were fed low chromium (−Cr, <0.15 μg/g diet) or chromium-adequate (+Cr, 2 μg Cr from CrCl3/g diet) casein-based diets and were restricted to 0.5 mg ascorbate/d (−C) or supplemented with 10 mg ascorbate/d (+C) for 23 weeks. Ascorbate depletion did not inhibit 51Cr uptake as evidenced by no difference in tissue retention and by a significant increase in urinary excretion in −C animals. Animals fed −Cr diets had higher 51Cr in blood and liver than those fed +Cr diets. An effect of previous dietary intake of chromium on 51Cr uptake has not been previously reported.
    Nutrition Research 10/1992; 12(10-12):1229-1234. DOI:10.1016/S0271-5317(05)80779-1 · 2.59 Impact Factor
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    ABSTRACT: Thirty-four weanling male rats were depleted of vitamin A and selenium for 5 wk, randomly assigned to groups in a 2 {times} 2 factorial design, and fed a torula yeast diet without vitamin A for 4 wks. The diets contained either 20 ppb Se ({minus}Se) or 510 ppb Se as sodium selenate (+Se) and 1 ppm Cu ({minus}Cu) or 6 ppm Cu (+Cu). Rats were fed 100 ug of beta-carotene daily. Force to break tibias was measured with a three point bending fixture in an Instron universal testing machine. Bone weights and kg force to break bones were increased by +Cu diets. Animals fed the {minus}Cu diets had depressed body and organ weights. An interaction between Cu and Se affected hepatic and kidney vitamin A after feeding carotene. Total hepatic vitamin A was 26.8, 44.2, 45.1 and 32.5 ug for the {minus}Cu{minus}Se, {minus}Cu+Se, +Cu{minus}Se, and +Cu+Se groups, respectively. Total kidney vitamin A was 8.7, 3.9, 7.1 and 13.5 ug for the same groups. Beta-carotene dioxygenase activity was not significantly affected by treatment. The findings indicate that dietary Cu and Se affect the metabolism of vitamin A.
    03/1991
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    ABSTRACT: Sixty-six weanling male rats were fed torula-yeast based diets and deprived of selenium, vitamin A and tocopherol for five weeks. Subsequently a two-factor central composite response surface experimental design was used to determine Se and tocopherol supplementation for nine groups. Selenium, as sodium selenate, was added to the diets at concentrations between 0 and 1.0 ppm. Rats were dosed with 0.2 to 50 mg/day of dl-alpha-tocopherol. All animals were fed 100 ug beta-carotene daily. Body, liver, and spleen weights were not significantly affecteds ofdietary treatments. Dietary Se affected heart weight. Hepatic vitamin A decreased linearly with increasing tocopherol supplements. In the combinations used, tocopherol decreased total vitamin A in liver and kidney but did not interact significantly with Se.
    The FASEB Journal 01/1991; 5(5). · 5.48 Impact Factor
  • C D Seaborn, E D Mitchell, B J Stoecker
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    ABSTRACT: Vanadium has been reported to affect numerous physiological processes; however, a demonstration that vanadium deficiency consistently impairs biological function is lacking. The purpose of this study was to determine if the activity of hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme in cholesterol synthesis, is affected by dietary supplementation of vanadate and/or chronic ascorbic acid deficiency. To determine if vanadium and/or ascorbic acid affected mineral metabolism, tissue minerals also were analyzed. Weanling male guinea pigs were assigned randomly to groups of 10 in a 2 x 2 factorial design. The dietary variables were ascorbate, 0.5 or 10 mg/day, and vanadium < 0.01 microgram or 0.5 microgram/g diet as NH4VO3 in a low Cr diet containing < 0.07 microgram Cr/g diet. After 21 weeks on this diet, guinea pigs receiving more ascorbate had lower liver weight/body weight ratios and increased bone copper. Testes weight/body weight ratios, hepatic glycogen and bone copper decreased while hepatic lipids, fecal bile acids, plasma cortisol and bone calcium and magnesium were increased by vanadium supplementation. An interaction between vanadium and ascorbate affected cholesterol excretion in feces, hepatic iron, plasma cholesterol concentration and the activity of HMG CoA reductase. This study provides evidence of increased bone mineral concentrations with vanadium supplementation and of an interaction between vanadium and ascorbate which affected cholesterol metabolism.
    Magnesium and trace elements 01/1991; 10(5-6):327-38.
  • Carol D. Seaborn, Barbara J. Stoecker
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    ABSTRACT: Absorption of trivalent chromium is low. Unbound chromium can form insoluble complexes in the gastrointestinal tract. In this study, effects of a calcium-based antacid or ascorbic acid on 51chromium from chromium chloride were investigated. Rats were dosed with 1 mL of test substance (containing 150 mg calcium carbonate or 10 mg ascorbic acid) or 1 mL water followed by 20 uCi 51chromium chloride. Twenty-four hours after dosing, 51chromium in cumulative urine was higher (p<0.02) in the group dosed with ascorbic acid than in the groups dosed with antacid or water. Accumulation of 51chromium in the kidney, testes, and spleen was lower (p<0.05) in rats dosed with antacid than in those dosed with ascorbic acid or water. These data confirm that absorption of chromium chloride is low and suggest that antacids have a negative effect on chromium absorption from chromium chloride.
    Nutrition Research 12/1990; 10(12):1401-1407. DOI:10.1016/S0271-5317(05)80132-0 · 2.59 Impact Factor
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    C D Seaborn, B J Stoecker
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    ABSTRACT: Forty-eight male genetically obese (OB) mice (C57BL/6J-OB) and 48 lean male littermates were randomly assigned within main plots (OB or lean) to one of eight diets. Diets were low chromium or supplemented with 1 mg chromium as CrCl3 per kg. Starch, sucrose, fructose or glucose comprised 50% of the diet, which met AIN recommendations except for chromium. Experimental diets and deionized water were available ad libitum for 26 d. Mice were fasted 10 h and were intubated 2 h before killing with 15 microCi of 51CrCl3 in a 25% carbohydrate solution (2 mg carbohydrate/g body wt) of either starch, sucrose, glucose or fructose corresponding to the diet previously fed. 51Cr concentrations were significantly higher in the blood, liver, spleen, epididymal fat pad, testes and femur of animals given their carbohydrate load as starch than in animals fed sucrose, fructose or glucose. Carbohydrate had a significant effect on chromium concentrations of testes, spleen, kidney and liver with values generally being higher with the starch diet. Chromium supplementation increased bone and kidney chromium concentrations and heart and muscle glycogen. These data indicate that the source of carbohydrate can alter chromium absorption and retention.
    Journal of Nutrition 11/1989; 119(10):1444-51. · 4.23 Impact Factor
  • Carol D. Seaborn, Forrest H. Nielsen

Publication Stats

288 Citations
36.96 Total Impact Points

Institutions

  • 2002–2003
    • University of Wisconsin - Stout
      Menominee, Wisconsin, United States
  • 1989–1995
    • Oklahoma State University - Stillwater
      • Department of Nutritional Sciences
      SWO, Oklahoma, United States
  • 1994
    • University of North Dakota
      Grand Forks, North Dakota, United States