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1.
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. 相似文献
2.
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 μg Si/g, respectively, based on ground
corn and casein, and supplemented with either 0 or 10 μg 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 μCi/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.
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 US Department
of Agriculture and does not imply its approval to the exclusion of other products that may be suitable. 相似文献
3.
《Archives of animal nutrition》2013,67(6):486-496
The present study investigated the effects of dietary sodium on bone growth in young rats. Five-week-old rats were fed one of three different diets for 60 days: low sodium (NaCl, 0.32 g/kg diet), normal sodium (NaCl, 2.6 g/kg) and high sodium (NaCl, 20 g/kg). The proximal tibial metaphysis (PTM), the fifth lumbar vertebra (LV5) and the middle part of the tibia shaft (TX) were analysed by bone histomorphometry. The expression of three osteogenesis genes, Runx2, osteopontin and osteocalcin, was determined by RT-PCR in bone samples from the skull. In both the PTM and LV5, trabecular area and thickness were increased by the low-sodium diet, while the high-sodium diet decreased trabecular area in LV5. Dynamic data revealed that sodium restriction increased bone formation parameters in the PTM and LV5, but decreased bone resorption in LV5. In TX, endosteal bone formation was enhanced by the low-sodium diet and depressed by the high-sodium diet compared to the normal sodium group. But there were no statistically changes in the cortical bone area of TX. Low-sodium intake significantly enhanced the expression of all three osteogenesis genes compared to the normal sodium group, while high-sodium intake suppressed osteogenic gene expression. Our results suggest that sodium restriction in growing rats promotes bone development by influencing both bone formation and resorption. 相似文献
4.
Curtiss D. Hunt Edward S. Halas Marilou J. Eberhardt 《Biological trace element research》1988,16(2):97-113
The purpose of this study was threefold: 1. to determine the long-term effects of interactions between lactational zinc deficiency
and gender on bone mineral composition in repleted rat offspring, 2. to determine the nutritional efficacy of the second of
two commercially designed, modified Luecke diets (ML2) during the gestational and lactational stress, and 3. determine the
ultratrace element contents of Ralston Rodent Laboratory Chow #5001. The ML2 basal diet, based on dextrose, sprayed egg white,
and corn oil contained 0.420 μg Zn/g, was supplemented with Zn (as zinc acetate) at 0 (diet 0ML2) or 30 (diet 30ML2) μg/g,
and was mixed and pelleted commercially. all rat dams were fed the 30ML2 diet ad libitum during gestation. Beginning at parturition,
the dams were fed either the 1. 0ML2, 2. 30ML2 (food restricted), or 3. 30ML2 (ad libitum) diets. All pups were fed the 30ML2
diet ad libitum from 23 to 40 d of age. From d 40 to 150, all pups were fed Ralston Rodent Laboratory Chow. The 30ML2 diet
was found to be nutritionally efficacious; litter size and pup growth were normal and pup mortality was only 1.2%. Pups (ZD)
with access to the 0ML2 diet until 23 d of age and nursed by dams fed the 0ML2 diet, when compared to pups (PF) fed restricted
amounts of the 30ML2 diet, exhibited increased mortality and decreased concentrations of tibial zinc but no change in growth.
Inadequate zinc nutriture during infancy, despite postlactational zinc repletion, induced imbalances in adult bone mineral
metabolism. Thus, at 150 d of age, the ZD pups exhibited increased levels of bone P and Mg and decreased concentrations of
K as compared to the PF pups. 相似文献
5.
Forrest H. Nielsen Terrence R. Shuler Thomas J. Zimmerman Eric O. Uthus 《Biological trace element research》1988,17(1):91-107
A series of nine experiments were done to obtain further evidence that boron might be involved in major mineral metabolism
(Ca, P, and Mg), thus indicating that boron is an essential nutrient for animals. Eight factorially arranged experiments of
6–10 wk durations were done with weanling Sprague-Dawley male rats. One factorially arranged experiment was done with weanling
spontaneously hypertensive rats. The variables in each experiment were dietary boron supplements of 0 and 3 μg/g, and dietary
magnesium supplements of either 200 (Experiments 1–3) or 100 (Experiments 4–9) and 400 μg/g. In Experiments 7 and 9, a third
variable was dietary manganese supplements of 25 and 50 μg/g. Methionine status was varied throughout the series of experiments
by supplementing the casein-based diet with methionine and arginine. Findings were obtained indicating that the severity of
magnesium deprivation and the methionine status of the rat strongly influence the extent and nature of the interaction between
magnesium and boron, and the response to boron deprivation. When magnesium deprivation was severe enough to cause typical
signs of deficiency, a significant interaction between boron and magnesium was found. Generally, the interaction was characterized
by the deprivation of one of the elements making the deficiency signs of the other more marked. The interaction was most evident
when the diet was not supplemented with methionine and especially when the diet contained luxuriant arginine. Signs of boron
deprivation were also more marked and consistent when the diet contained marginal methionine and luxuriant arginine. Among
the signs of boron deprivation exhibited by rats fed marginal methionine were depressed growth and bone magnesium concentration,
and elevated spleen wt/body wt and kidney wt/body wt ratios. Because the boron supplement of 3 μg/g did not make the dietary
intake of this element unusual, it seems likely that the response of the rats to dietary boron in the present study were manifestations
of physiological, not pharmacological, actions, and support the hypothesis that boron is an essential nutrient for the rat.
Mentions of a trademark or proprietary product does not consitute a guarantee or warranty of the product by the US Department
of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable. 相似文献
6.
Forrest H. Nielsen Thomas J. Zimmerman Terrence R. Shuler 《Biological trace element research》1982,4(2-3):125-143
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. 相似文献
7.
The level and/or form of dietary iron, dietary nickel, and the interaction between them affected the trace element content
of rat liver. Livers were from the offspring of dams fed diets containing 10–16 ng, or 20 μg, of nickel/g. Dietary iron was
supplied as ferric chloride (30 μg/g) or ferric sulfate (30 μg, or 60 μg). In nickel-deprived rats fed 60 μg of iron/g of
diet as ferric sulfate, at age 35 days, levels of iron and zinc were depressed in liver and the level of copper was elevated.
At age 55 days, iron was still depressed, copper was still elevated, but zinc also was elevated. In rats fed 30 μg of iron/g
of diet as ferric chloride, liver iron content was higher in nickel-deprived than in nickel-supplemented rats at 30, but not
at 50, days of age. Also manganese and zinc were lower in nickel-deprived than in nickel-supplemented rats at age 35 days
if their dams had been on experiment for an extended period of time (i.e., since age 21 days). Thus, the levels of copper,
iron, manganese, and zinc in liver were affected by nickel deprivation, but the direction and extent of the affects depended
upon the iron status of the rat. 相似文献
8.
Nielsen FH 《BioFactors (Oxford, England)》2004,20(3):161-171
Female and male rats weighing about 170 g and 200 g, respectively, were fed diets (approximately 70 microg boron/kg) in a factorial arrangement with supplemental boron at 0 (deficient) and 3 (adequate) mg/kg and canola oil or palm oil at 75 g/kg of diet as variables. After 5 weeks, six females in each treatment were bred. Dams and pups continued on their respective dietary treatments through gestation, lactation and post-weaning. Thirteen weeks after weaning, plasma and bones were collected from 12 male and 12 female offspring in each treatment. Boron supplementation increased femur strength measured by the breaking variable bending moment; tibial calcium and phosphorus concentrations; and plasma alkaline phosphatase. Femur breaking stress was greatest in boron-supplemented rats fed canola oil, and lowest in boron-deprived females fed canola oil; this group also exhibited the lowest femur bending moment. Minerals associated with bone organic matrix, zinc and potassium, were increased by boron supplementation in tibia. Plasma phospholipids were decreased by boron deprivation in females, but not males. Plasma cholesterol was decreased in boron-supplemented males by replacing canola oil with palm oil. The findings suggest that a diet high in omega-3 alpha-linolenic acid promotes femur strength best when the dietary boron is adequate. 相似文献
9.
Forrest H. Nielsen Terrence R. Shuler Thomas J. Zimmerman Michael E. Collings Eric O. Uthus 《Biological trace element research》1979,1(4):325-335
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. 相似文献
10.
The use of hair and bone as media in evaluation of lead exposure was investigated in this study. For 12–16 wk rats were given
tap water containing lead acetate in the following concentrations: 41.7 mg Pb/L, 83.3 mg Pb/L, and 166.6 mg Pb/L. The animals
were sacrificed every 4 wk and their tibia bones and hair were collected for determination of lead content. In control animals,
the lead level amounted to 1.2 μg/g (range 0.8–1.3 μg/g) and 0.7 μg/g (range 0.4–2.0 μg/g) in bone and hair, respectively.
In the treated rats the accumulation of lead in bone and hair occurred in a dose-dependent manner. A positive corelation (r=0.876) was established between the lead levels in bone and hair of the rats. The regression equation was as follows: μg Pb/g
bone=0.842×μg Pb/g hair+1.868. After discontinuation of exposure, a significant decrease in the lead content in bone and hair
was noticed. About 9 wk after cessation of treatment, the lead content in hair declined to the pre-exposure level, but 64%
of the maximal lead concentration did remain in bone. The results of this study indicate that during a continuous exposure
the lead level in hair reflects its content in bone. Such phenomena did not occur during the postexposure period. 相似文献
11.
The present study investigated the effects of dietary sodium on bone growth in young rats. Five-week-old rats were fed one of three different diets for 60 days: low sodium (NaCl, 0.32 g/kg diet), normal sodium (NaCl, 2.6 g/kg) and high sodium (NaCl, 20 g/kg). The proximal tibial metaphysis (PTM), the fifth lumbar vertebra (LV5) and the middle part of the tibia shaft (TX) were analysed by bone histomorphometry. The expression of three osteogenesis genes, Runx2, osteopontin and osteocalcin, was determined by RT-PCR in bone samples from the skull. In both the PTM and LV5, trabecular area and thickness were increased by the low-sodium diet, while the high-sodium diet decreased trabecular area in LV5. Dynamic data revealed that sodium restriction increased bone formation parameters in the PTM and LV5, but decreased bone resorption in LV5. In TX, endosteal bone formation was enhanced by the low-sodium diet and depressed by the high-sodium diet compared to the normal sodium group. But there were no statistically changes in the cortical bone area of TX. Low-sodium intake significantly enhanced the expression of all three osteogenesis genes compared to the normal sodium group, while high-sodium intake suppressed osteogenic gene expression. Our results suggest that sodium restriction in growing rats promotes bone development by influencing both bone formation and resorption. 相似文献
12.
Effects of boric acid supplementation on bone histomorphometry,metabolism, and biomechanical properties in aged female F-344 rats 总被引:1,自引:0,他引:1
Gallardo-Williams MT Maronpot RR Turner CH Johnson CS Harris MW Jayo MJ Chapin RE 《Biological trace element research》2003,93(1-3):155-169
Postmenopausal women may benefit from dietary interventions in order to increase bone strength and prevent fractures. Dietary
boron (B) may be beneficial for optimal calcium metabolism and, as a consequence, optimal bone metabolism. The present study
evaluated the effects of boron, in the form of boric acid, with or without 17β-estradiol (E2) supplementation (via subcutaneous implant), in ovariectomized (OVX) aged 13-mo-old F-344 rats. Boric acid was administered
by gavage at a subtoxic dose (8.7 mg B/kg/d) for 40 d. Results indicate that serum level of minerals as well as osteocalcin
(a marker of bone resorption) are dependent to a greater extent on the hormonal status of the animals than on boron supplementation.
Boron treatment increased the E2-induced elevation of urinary calcium and magnesium. Bone mineral density (BMD) of the L5 vertebra and proximal femur was
highest in the E2-treated groups; no increase in BMD was conferred by boron treatment. By histomorphometry of the proximal tibial metaphysis,
osteoblastic, osteoid, and eroded surfaces were significantly suppressed by E2 treatment, but not by boron treatment. In biomechanical testing of femur and vertebra, neither E2 nor boron treatment significantly increased bone strength. At the levels given, boron alone provided no protection against
OVX-induced osteopenia. In addition, combination therapy (B + E2) provided no additional benefits over those of 17β-estradiol treatment alone in this aged rat model. 相似文献
13.
Huawei Zeng Eric O. Uthus Sharon A. Ross Cindy D. Davis 《Biological trace element research》2009,131(1):71-80
Our previous studies have shown that selenium (Se) is protective against dimethylhydrazine (DMH)-induced preneoplastic colon
cancer lesions, and protection against DNA damage has been hypothesized to be one mechanism for the anticancer effect of Se.
The present study was designed to determine whether dietary selenite affects somatic mutation frequency in vivo. We used the
Big Blue transgenic model to evaluate the in vivo mutation frequency of the cII gene in rats fed either a Se-deficient (0 μg Se/g diet) or Se-supplemented diet (0.2 or 2 μg Se/g diet; n = 3 rats/diet in experiment 1 and n = 5 rats/group in experiment 2) and injected with DMH (25 mg/kg body weight, i.p.). There were no significant differences
in body weight between the Se-deficient and Se-supplemented (0.2 or 2 μg Se/g diet) rats, but the activities of liver glutathione
peroxidase and thioredoxin reductase and concentration of liver Se were significantly lower (p < 0.0001) in Se-deficient rats compared to rats supplemented with Se. We found no effect of dietary Se on liver 8-hydroxy-2′-deoxyguanosine.
Gene mutation frequency was significantly lower in liver (p < 0.001) than that of colon regardless of dietary Se. However, there were no differences in gene mutation frequency in DNA
from colon mucosa or liver from rats fed the Se-deficient diet compared to those fed the Se-supplemented (0.2 or 2 μg Se/g
diet) diet. Although gene mutations have been implicated in the etiology of cancer, our data suggest that decreasing gene
mutation is not likely a key mechanism through which dietary selenite exerts its anticancer action against DMH-induced preneoplastic
colon cancer lesions in a Big Blue transgenic rat model.
The US Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative
action employer and all agency services are available without discrimination.
Mention of a trademark or proprietary product does not constitute a guarantee or warranty of the product by the US Department
of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable.
This work was supported by the US Department of Agriculture and National Cancer Institute. 相似文献
14.
Cell culture studies have suggested that arsenic exposure results in decreased S-adenosylmethionine (SAM), causing DNA hypomethylation. Previously, we have shown that hepatic SAM is decreased and/or S-adenosylhomocysteine increased in arsenic-deprived rats; these rats tended to have hypomethylated DNA. To determine, the
effect of dietary arsenic on dimethylhydrazine (DMH)-induced aberrant crypt formation in the colon, Fisher 344 weanling male
rats were fed diets containing 0,05, or 50 μg As (as NaAsO2)/g. After 12 wk, dietary arsenic affected the number of aberrant crypts (p<0.02) and aberrant crypt foci (p<0.007) in the colon and the amount of global DNA methylation (p<0.04) and activity of DNA methyltransferase (DNMT) (p<0.003) in the liver. In each case, there were more aberrant crypts and aberrant crypt foci, a relative DNA hypomethylation,
and increased activity of DNMT in the rats fed 50 μg As/g compared to those fed 0.5 μg As/g. The same phenomenon, an increased
number of aberrant crypts and aberrant crypt foci, DNA hypomethylation, and increased DNMT tended to hold when comparing rats
fed the diet containing no supplemental arsenic compared to rats fed 0.5 μg As/g. The data suggest that there is a threshold
for As toxicity and that possibly too little dietary As could also be detrimental.
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. 相似文献
15.
Assessing the effects of low boron diets on embryonic and fetal development in rodents using in vitro and in vivo model systems 总被引:2,自引:0,他引:2
Lanoue L Taubeneck MW Muniz J Hanna LA Strong PL Murray FJ Nielsen FH Hunt CD Keen CL 《Biological trace element research》1998,66(1-3):271-298
To date, boron (B) essentiality has not been conclusively shown in mammals. This article summarizes the results of a series
of in vitro and in vivo experiments designed to investigate the role of B in mammalian reproduction. In the first study, rat
dams were fed either a low (0.04 μg B/g) or an adequate (2.00 μg B/g) B diet for 6 wk before breeding and through pregnancy;
reproductive outcome was monitored on gestation day 20. Although low dietary B significantly lowered maternal blood, liver,
and bone B concentrations, it had no marked effects on fetal growth or development. The goal of the second study was to assess
the effects of B on the in vitro development of rat postimplantation embryos. Day 10 embryos collected from dams fed either
the low or adequate B diets for at least 12 wk were cultured in serum collected from male rats exposed to one of the two dietary
B treatments. Dams fed the low B diet had a significantly reduced number of implantation sites compared to dams fed the B-adequate
diet. However, embryonic growth in vitro was not affected by B treatment. The aim of study 3 was to define the limits of boric
acid (BA) toxicity on mouse preimplantation development in vitro. Two-cell mouse embryos were cultured in media containing
graded levels of BA (from 6 to 10,000 μM). Impaired embryonic differentiation and proliferation were observed only when embryos
were exposed to high levels of BA (>2000 μM), reflecting a very low level of toxicity of BA on early mouse embryonic development.
Study 4 tested the effects of low (0.04 μg B/g) and adequate (2.00 μg B/g) dietary B on the in vitro development of mouse
preimplantation embryos. Two-cell embryos obtained from the dams were cultured in vitro for 72 h. Maternal exposure to the
low B diet for 10, 12, and 16 wk was associated with a reduction in blastocyst formation, a reduction in blastocyst cell number,
and an increased number of degenerates. Collectively, these studies support the concept that B deficiency impairs early embryonic
development in rodents. 相似文献
16.
Forrest H. Nielsen 《Biological trace element research》2010,135(1-3):45-55
An experiment with rats was conducted to determine whether silicon deprivation affects the acute-phase immune response to an endotoxin challenge. Weanling female rats were assigned to two weight-matched groups of 24; one group was fed a basal diet containing about 1.9 µg Si/kg; the other group was fed the basal diet supplemented with 35 µg Si/kg as arginine silicate inositol complex. After being fed their respective diets for 8 weeks, 12 rats in each group were injected subcutaneously with 1 mg lipopolysaccharide (LPS)/kg body weight; the other 12 rats in each group were injected with deionized water. Two hours after injection, the rats were anesthetized with ether for collection of blood (for plasma), liver and femurs, and then euthanized by decapitation. LPS injection decreased total white blood cell, lymphocyte, monocyte, eosinophil, and basophil counts by 80–90%, but did not affect neutrophil counts. LPS injection also increased plasma tumor necrosis factor-α and osteopontin and decreased plasma hyaluronic acid. Silicon deprivation did not significantly affect any of these responses to LPS. Silicon in liver and silicon, iron, and zinc in femur were increased by LPS injection only in silicon-deprived rats. Silicon deprivation also increased monocyte counts and osteopontin and decreased femur zinc in rats not injected with LPS. The findings indicate that silicon deprivation does not affect the acute-immune phase decrease in inflammatory cell numbers and increase in inflammatory cytokines in response to an endotoxin challenge. Silicon deprivation, however, apparently causes slight chronic inflammation and might influence inflammatory cell proliferation in the chronic-phase inflammatory response. 相似文献
17.
Forrest H. Nielsen Barbara J. Stoecker 《Journal of trace elements in medicine and biology》2009,23(3):195-203
An experiment was performed to determine whether boron deprivation would adversely affect vertebra (trabecular) bone microarchitecture, and whether any adverse effect would be modified by dietary fatty acid composition. Female rats were fed diets containing 0.1 mg (9 μmol) boron/kg in a factorial arrangement with variables of supplemental boron at 0 (boron-deprived) or 3 (boron-adequate) mg (278 μmol)/kg and fat sources of 75 g safflower oil/kg or 65 g fish (menhaden) oil/kg plus 10 g linoleic acid/kg. After 6 weeks, six females per treatment were bred. Dams and pups continued on their respective diets through gestation, lactation, and after weaning. At age 21 weeks, the microarchitecture of the fourth lumbar vertebrae from 12 randomly selected pups from each treatment was determined by microcomputed tomography. Boron deprivation decreased bone volume fraction and increased trabecular separation and structural model index. Boron deprivation decreased trabecular thickness when the dietary oil was safflower. A three-point bending test for bone strength found that boron deprivation decreased the maximum force needed to break the femur. Feeding fish oil instead of safflower oil decreased connectivity density in vertebrae of boron-deficient but not in boron-adequate rats. Fish oil instead of safflower oil increased the maximum force to break and the bending moment of the femur, especially in rats fed adequate boron. The findings confirm that boron and fish oil are beneficial to cortical bone strength, and show that nutritional intakes of boron are beneficial for trabecular bone microarchitecture and influence the beneficial effects of fish oil on bone. 相似文献
18.
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. 相似文献
19.
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. 相似文献
20.
Interleukin-10-/- (IL-10) knockout (KO) mice develop an intestinal inflammation that closely mimics human inflammatory bowel disease (IBD) which is accompanied by inflammation-associated bone abnormalities and elevated serum proinflammatory cytokines. The objective of this study was to use the IL-10 KO mouse model to determine whether flaxseed oil (FO) diet, rich in alpha-linolenic acid (ALA), attenuates intestinal inflammation and inflammation-associated bone abnormalities, compared to a corn oil (CO) control diet. Male wild-type (WT) or IL-10 KO mice were fed a 10% CO or 10% FO diet from weaning (postnatal day 28) for 9 weeks. At necropsy, serum, intestine, femurs and lumbar vertebrae were collected and analyzed. IL-10 KO mice fed CO had lower femur bone mineral content (BMC; P<.001), bone mineral density (BMD; P<.001), peak load (P=.033) and lumbar vertebrae BMD (P=.02) compared to WT mice fed either diet. Flaxseed oil had a modest, favorable effect on IL-10 KO mice as femur BMC, BMD and peak load were similar to WT mice fed CO or FO. In addition, lumbar vertebra BMD was similar among IL-10 KO mice fed FO and WT mice fed CO or FO. The fact that FO attenuated serum tumor necrosis factor-alpha (TNF-alpha) among IL-10 KO mice suggests that the positive effects of FO on femur BMC, BMD, peak load and vertebral BMD in IL-10 KO mice may have been partly mediated by changes in serum TNF-alpha. In conclusion, these findings suggest that a dietary level of ALA attainable from a 10% flaxseed oil diet results in modest improvements in some bone outcomes but does not attenuate intestinal inflammation that is characteristic of IL-10 KO mice. 相似文献