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  • 1
    Electronic Resource
    Electronic Resource
    Influence of short-term aluminum exposure on demineralized bone matrix induced bone formation (1992)
    Springer
    Archives of toxicology 66 (1992), S. 706-712 
    Details
    ISSN: 1432-0738
    Keywords: Aluminum ; Bone formation ; Cartilage ; Calcification ; Osteogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of aluminum exposure on bone formation employing the demineralized bone matrix (DBM) induced bone development model were studied using 4-week-old Sprague-Dawley rats injected with a saline (control) or an aluminum chloride (experimental) solution. After 2 weeks of aluminum treatment, 20-mg portions of rat DBM were implanted subcutaneously on each side in the thoracic region of the control and experimental rats. Animals were killed 7, 12, or 21 days after implantation of the DBM and the developing plaques removed. No morphological, histochemical, or biochemical differences were apparent between plaques from day 7 control and experimental rats. Plaques from day 12 control and experimental rats exhibited cartilage formation and alkaline phosphatase activity localized in osteochondrogenic cells, chondrocytes, osteoblasts, and extracellular matrix. Unlike the plaques from control rats that contained many osteoblastic mineralizing fronts, the plaques from the 12-day experimental group had a preponderance of cartilaginous tissue, no evidence of mineralization, increased levels of alkaline phosphatase activity, and a reduced calcium content. Plaques developing for 21 days in control animals demonstrated extensive new bone formation and bone marrow development, while those in the experimental rats demonstrated unmineralized osteoid-like matrix with poorly developed bone marrow. Alkaline phosphatase activity of the plaques continued to remain high on day 21 for the control and experimental groups. Calcium levels were significantly reduced in the experimental group. These biochemical changes correlated with histochemical reductions in bone calcification. Thus, aluminum administration to rats appears to alter the differentiation and calcification of developing cartilage and bone in the DBM-induced bone formation model and suggests that aluminum by some mechanism alters the matrix calcification in growing bones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01972621
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  • 2
    Electronic Resource
    Electronic Resource
    Aluminum toxicity perturbs long bone calcification in the embryonic chick (1999)
    Springer
    Archives of toxicology 73 (1999), S. 359-366 
    Details
    ISSN: 1432-0738
    Keywords: Key words Aluminum toxicity ; Embryonic bone ; Bone calcification ; Collagen ; Alkaline phosphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Long bone calcification in chick embryos acutely- or chronically-treated with aluminum (Al) citrate was investigated. Acutely treated embryos received 100 μl of 60 mM Al citrate, 60 mM sodium (Na) citrate, or 0.7% sodium chloride on day 8 of incubation. Chronically treated embryos received a daily 25 μl dose of the above solutions beginning on day 8. Following 2–8 days of additional incubation, blood was collected, embryos killed, hind limbs radiographed, and tibias collected. Radiography indicated that Al administration resulted in a persistent angulation in the mid-diaphysis of tibias and femurs and a transient mineralization defect during the 10- to 12-day period of incubation. Tibias from 10- to 12-day embryos which were administered Al contained significantly less (P 〈 0.005) bone calcium (Ca) compared with tibias from NaCl-treated embryos. By day 14 there were no significant differences among the Ca content of tibias from embryos acutely treated with Al citrate, Na citrate or NaCl. Similarly, the rate of 45Ca uptake by tibias of embryos treated with Al was significantly lower on days 10 (acute) and 12 (chronic) with no significant differences in Ca uptake rate among the three treatment groups by day 16. In each treatment group bone alkaline phosphatase (ALPase) activity increased approximately tenfold between days 10 and 16. At all stages, bone ALPase activity was consistently higher and significantly different (chronic) compared with levels in NaCl-treated embryos. In contrast, Al had no significant effect on the rate of tibia collagen and noncollagenous protein synthesis or serum levels of procollagen carboxy-terminal propeptide (PICP), osteocalcin, and parathyroid hormone (PTH).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050674
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  • 3
    Electronic Resource
    Electronic Resource
    Aluminum effects on blood chemistry and long bone development in the chick embryo (1994)
    Springer
    Archives of toxicology 68 (1994), S. 541-547 
    Details
    ISSN: 1432-0738
    Keywords: Key words: Aluminum toxicity  –  Chick embryo  –  Bone mineralization  –  Bone development  –  Citrate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Body growth, blood chemistry, and long bone development of 10- to 16-day chick embryos (Gallus gallus) treated with aluminum (Al) citrate, sodium (Na) citrate, or sodium chloride (NaCl) were investigated. Two administration protocols were used. Acutely-treated embryos received 6.0 μmol Al citrate or Na citrate on day 8 of incubation. Chronically-treated embryos received a daily dose of 1.5 μmol Al citrate or Na citrate beginning on day 8 of incubation. For both protocols, Al citrate and Na citrate had no significant influence on viability or body weight. Al citrate-treated embryos had: (a) significantly shorter mean tibia lengths by day 16 of incubation, (b) a consistently lower ratio of tibia length: body weight on all days investigated, and (c) a persistent mid-diaphyseal malformation (angulation) of the femur and tibia. Spatially correlated with the malformation was a calcification defect detected by alizarin red S staining of intact tibias and the accumulation of aluminum as demonstrated by acid solochrome azurine staining of histological sections. Aluminum was localized at the mineralization front of the osteogenic collar surrounding the cartilage core of the tibia. Aluminum citrate or Na citrate had no significant effect on serum total calcium, inorganic phosphorus, total alkaline phosphatase activity, or creatinine, except for a transitory hypercalcemia (day 10) and phosphatemia (days 10 and 12) in Al citrate-treated embryos. The concomitant localization of Al and the early calcification defect in the region of tibial malformation implicate aluminum in the pathogenesis of the skeletal abnormality.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050111
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  • 4
    Electronic Resource
    Electronic Resource
    3H-fucose incorporation into bone following exposure to parathyroid hormone, dibutyryl cyclic-AMP and colchicine (1981)
    Springer
    Cell & tissue research 214 (1981), S. 583-591 
    Details
    ISSN: 1432-0878
    Keywords: Fucose ; Bone ; Parathyroid hormone ; Adenosine cyclic monophosphate ; Colchicine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Radioautographic and scintillation counting procedures were used to examine the effect of parathyroid hormone (PTH), dibutyryl cyclic-AMP (DB-cAMP), and colchicine on the incorporation of 3H-fucose into macromolecular material in organ cultures of bone. Radioautography demonstrated 3H-fucose incorporation into bone cells, with the heaviest uptake occurring in osteoclasts. A minimal incorporation occurred in pre-osteoblasts and osteoblasts of the osteogenic periosteum, and in fibroblasts of the fibrous periosteum. PTH appeared to produce a heavier label in association with osteoclasts while decreasing the limited labeling associated with cells of the osteogenic and fibrous periosteum. DB-cAMP and colchicine both markedly reduced the labeling associated with osteoclasts, while the minimal labeling of other bone cells remained. By contrast, scintillation counting results indicated that PTH had little or no effect on 3H-fucose incorporation, while DB-cAMP and colchicine considerably reduced the amount of labeled macromolecular material. The incorporation of 3H-fucose into glycoproteins and the role of glycoproteins are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233498
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  • 5
    Electronic Resource
    Electronic Resource
    Colchicine stimulation of hyaluronate synthesis and secretion in bone organ culture (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 101 (1979), S. 341-348 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Parathyroid hormone (PTH) is known to have a number of effects on bone tissue in vitro, including the stimulation of calcium release and the synthesis and turnover of hyaluronate. PTH-stimulated calcium release is inhibited by colchicine. Since hyaluronate may play a role in demineralization, calcium release into the media as a measure of bone resorption was correlated with the synthesis and secretion of 3H-glucosamine-labeled macromolecules. Newborn mice were labeled with 45Ca, and the calvaria removed and incubated in vitro in media containing 3H-glucosamine. Addition of colchicine to the culture media inhibited the release of 45Ca into the media while stimulating the synthesis and secretion of 3H-glucosamine labeled macromolecules. DEAE-cellulose chromatography resolved the labeled macromolecular material into four peaks, of which the third peak containing hyaluronate demonstrated approximately twice the amount of radioactivity. PTH stimulation of calcium release was inhibited likewise by colchicine, while 3H-glucosamine incorporation into labeled macromolecules was stimulated. Short term labeling studies emphasized the marked stimulatory effect that both PTH and colchicine have on the incorporation of 3H-glucosamine into hyaluronate. PTH stimulated the incorporation of 35S-sulfate, while colchicine markedly inhibited its incorporation into non-dialyzable material. Both PTH and colchicine inhibited protein synthesis. Based on the observations, colchicine appears to stimulate the synthesis and secretion of hyaluronate and alter a number of metabolic pathways. Hyaluronate does not appear to be directly involved in the demineralization process.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041010213
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  • 6
    Electronic Resource
    Electronic Resource
    Localization and distribution of adenosine triphosphatase activity in the femurs of young miceResearch supported by NIH grants 2-F2-AM-30; FR 5332-06, and the U. S. Atomic Energy Commission.Presented in part at the 80th Annual Meeting of the American Association of Anatomists, Kansas City, Mo., April 1967. (1968)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 161 (1968), S. 57-67 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The localization and distribution of ATPase activity in the femurs of young mice was evaluated using the lead-ATPase histochemical method. The skeletal system demonstrated an intracellular distribution of ATPase activity. Enzyme activity of osteoclasts, and metaphyseal and perichondrial osteoblasts was high. Endosteal and periosteal osteoblasts varied in activity depending upon the area under observation. Preosteoblasts (progenitive cells) of the osteogenic periosteum, osteochondrogenic cells of the perichondrial region, chondrocytes, and cells of the fibrous periosteum demonstrated minimal activity. Osteocytes were negative. The distribution of osteoblast APTase activity coincided with areas of active collagen synthesis.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091610106
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  • 7
    Electronic Resource
    Electronic Resource
    Changes in distribution of lipid, glucose-6-phosphate dehydrogenase and malate enzyme within the liver lobule of the rat during adaptive hyperlipogenesis (1973)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 175 (1973), S. 231-241 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Feeding rats a high-sucrose, fat-free diet after two days of starvation resulted in an initial accumulation of hepatic lipid and an increased activity of those enzymes which catalyze and support the formation of fatty acids from acetyl precursors. Rats starved for 48 hours were refed a high-carbohydrate, fat-free diet for 1, 2, 3, 5, 7 and 14 days. Frozen sections of liver were stained with Oil Red O for lipids. In adjacent sections glucose-6-phosphate dehydrogenase (GDH)and malate enzyme (ME) were localized and the relative enzyme activity evaluated. Enlargement and yellowing of the liver were noted after two to three days feeding of the fat-free diet, but subsequently the liver appeared normal. Oil Red O staining demonstrated a progressive accumulation of lipid from the periportal to the centrilobular area during the first three days of refeeding. After the seventh day on the fat-free diet, however, the lipid accumulation was less and the distribution appeared similar to that of animals maintained on a balanced diet. A marked increase in both GDH and ME activity was noted throughout the liver lobule after two days on the fat-free diet. Enzyme activity remained high throughout the lobule during the balance of the experimental period, with maximum activity in the centrilobular area.
    Additional Material: 1 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091750207
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