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  • Electronic Resource  (2)
  • 3H-25 hydroxyvitamin D  (1)
  • Alcohol  (1)
  • 1
    ISSN: 1432-0827
    Keywords: Alcohol ; Electron microscopy ; Growth plate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We have previously demonstrated that ethanol has a direct toxic effect on the rat skeleton characterized by decreased trabecular bone volume. In the present study, we examined the ultrastructure of the distal radial epiphyseal growth plates in these same animals. Eight weeks of ethanol administration to 12 male rats results in serum alcohol levels of 140 mg/dl but did not alter the width or light microscopic appearance of the radial growth plate. Quantitative electron microscopy failed to demonstrate morphologic evidence of toxicity in the skeletal cells. We conclude that although ethanol appears to have a direct effect on rat bone characterized by enhanced resorption, toxicity is not attended by ultrastructural changes in the skeletal cells.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 35 (1983), S. 461-464 
    ISSN: 1432-0827
    Keywords: Vitamin D metabolites ; Liver perfusion ; Liver homogenates ; 3H-25 hydroxyvitamin D
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of the vitamin D metabolites 1,25 dihydroxyvitamin D (100 pg/ml) and 25-hydroxyvitamin D (30 ng/ml) on hepatic production of3H-25 hydroxyvitamin D was investigated using rachitic liver perfusions and homogenates. 1,25 dihydroxyvitamin D inhibited hepatic3H-25 hydroxyvitamin D production in the liver perfusion (3.6 ± 0.4 vs 2.0 ± 0.5 pmol/liver,P〈0.05) and in liver homogenates (11.9 ± 0.6 vs 10.1 ± 0.4 pmol/g liver protein/3 h,P〈0.02). Inhibition was time and dose dependent. 25-hydroxyvitamin D inhibited production in liver homogenates (11.9 ± 0.6 vs 9.2 ± 0.1 pmol/g liver protein/3 h,P〈0.05) but not in the intact liver (3.6 ± 0.4 vs 3.4 ± 0.5 pmol/liver). The data indicate that 1,25 dihydroxyvitamin D is able to feedback regulate the production of its precursor, 25-hydroxyvitamin D. Although 25-hydroxyvitamin D also inhibits its own production in liver homogenates, it failed to alter total production in the intact liver, suggesting that this metabolite may require immediate access to the vitamin D 25-hydroxylase, located on the microsomes and mitochondria, to induce inhibition.
    Type of Medium: Electronic Resource
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