[Show abstract][Hide abstract] 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. · 1.31 Impact Factor
[Show abstract][Hide abstract] 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. · 1.31 Impact Factor
[Show abstract][Hide abstract] 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. · 1.31 Impact Factor
[Show abstract][Hide abstract] 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 12/2001; 15(3):113 - 122.
[Show abstract][Hide abstract] ABSTRACT: Circumstantial evidence suggests that aluminum, arsenic, bromine, cadmium, germanium, lead, lithium, nickel, rubidium, silicon, tin and vanadium are essential. The evidence is most compelling for arsenic, nickel, silicon and vanadium. The estimated daily dietary intakes for these elements are arsenic, 12-50 micrograms; nickel, 100 micrograms; silicon, 20-50 mg and vanadium, 10-20 micrograms. By extrapolation from animal studies, the daily dietary intakes of these elements needed to prevent deficiency or to provide beneficial action in humans are arsenic, 12-25 micrograms; nickel, 100 micrograms; silicon, 2-5 mg (based on 10% bioavailability in natural diets) and vanadium, 10 micrograms. Thus, the postulated need by humans for these elements can be met by typical diets. Because there may be situations, however, where dietary intake does not meet the postulated requirements, research is needed to derive status indicators in humans and to further study the relationships of low intake or impaired bioavailability of these ultratrace elements to various diseases.
Journal of Nutrition 10/1996; 126(9 Suppl):2452S-2459S. · 4.20 Impact Factor
[Show abstract][Hide abstract] 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. · 1.31 Impact Factor
[Show abstract][Hide abstract] 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. · 1.31 Impact Factor
[Show abstract][Hide abstract] 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; · 2.62 Impact Factor
[Show abstract][Hide abstract] 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. · 1.31 Impact Factor
[Show abstract][Hide abstract] 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.