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  • Cell & Developmental Biology  (5)
  • ATP synthesis  (3)
  • 1-aniline-8-naphathalene sulfonate fluorescence  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Heart FoF1-ATPase changes during the acute phase of Trypanosoma cruzi infection in rats (1996)
    Springer
    Molecular and cellular biochemistry 165 (1996), S. 127-133 
    Details
    ISSN: 1573-4919
    Keywords: Trypanosoma cruzi ; rat heart ; mitochondria ; oxidative phosphorylation ; FoF1-ATPase ; ATP hydrolysis ; ATP synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The kinetic properties of ATP hydrolysis and synthesis by FoF1-ATPase of heart mitochondria were evaluated during the acute phase of T. cruzi infection in rats. Mitochondria and submitochondrial particles were isolated 7 days (early stage) and 25 days (late stage) following infection of rats with 2 × 105 trypomastigote forms of the Y strain of T. cruzi. The kinetic properties for ATP hydrolysis were altered for the early but not the late stage, showing a changed pH profile, increased K0.5 values, and a decreased total Vmax. The Arrhenius' plot for membrane-associated enzyme showed a higher transition temperature with a lower value for the activation energy in body temperature. For the Triton X-100 - solubilized enzyme, the plot was similar to the control. A decrease in the efficiency of ADP phosphorylation by mitochondria, measured by the firefly-luciferase luminescence, was observed only during the late stage and appeared to be correlated with a decrease in the affinity of the FoF1-ATPase for ADP. It is proposed that in the early stage, during the acute phase of T. cruzi infection in rats, heart FoF1-ATPase undergoes a membrane-dependent conformational change in order to maintain the phosphorylation potential of mitochondria, which would compensate for the uncoupling of mitochondrial function. Also, during both the early and late stages, the enzyme seems to be under the regulation of the endogenous inhibitor protein for the preservation of cellular ATP levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229474
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  • 2
    Electronic Resource
    Electronic Resource
    Hg(II)-induced renal cytotoxicity: In vitro and in vivo implications for the bioenergetic and oxidative status of mitochondria (1997)
    Springer
    Molecular and cellular biochemistry 177 (1997), S. 53-59 
    Details
    ISSN: 1573-4919
    Keywords: mercury ; rat kidney ; mitochondria ; oxidative phosphorylation ; FoF1-ATPase ; ATP synthesis ; ATP hydrolysis ; oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effects of Hg(II) on bioenergetic and oxidative status of rat renal cortex mitochondria were evaluated both in vitro, and in vivo 1 and 24 h after treatment of animals with 5 mg HgCl2/kg ip. The parameters assessed were mitochondrial respiration, ATP synthesis and hydrolysis, glutathione content, lipid peroxidation, protein oxidation, and activity of antioxidant enzymes. At low concentration (5 µM) and during a short incubation time, Hg(II) uncoupled oxidative phosphorylation while at slightly higher concentration or longer incubation time the ion impaired the respiratory chain. The rate of ATP synthesis and the phosphorylation potential of mitochondria were depressed, although inhibition of ATP synthesis did not exceed 50%. In vivo, respiration and ATP synthesis were not affected 1 h post-treatment, but were markedly depressed 24 h later. ATP hydrolysis by submitochondrial particle FoF1-ATPase was inhibited (also by no more than 50%) both in vitro, and in vivo 1 and 24 h post-treatment. Hg(II) induced maximum ATPase inhibition at about 1 uM concentration but did not have a strong inhibitory effect in the presence of Triton X-100. Oxidative stress was not observed in mitochondria 1 h post-treatment. However, 24 h later Hg(II) reduced the GSH/GSSG ratio and increased mitochondrial lipid peroxidation and protein oxidation, as well as inhibited GSH-peroxidase and GSSG-reductase activities. These results suggest that the following sequence of events may be involved in Hg(II) toxicity in the kidney: (1) inhibition of FoFl-ATPase, (2) uncoupling of oxidative phosphorylation, (3) oxidative stress-associated impairment of the respiratory chain, and (4) inhibition of ATP synthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006861319378
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  • 3
    Electronic Resource
    Electronic Resource
    Fluoxetine interacts with the lipid bilayer of the inner membrane in isolated rat brain mitochondria, inhibiting electron transport and F1F0-ATPase activity (1999)
    Springer
    Molecular and cellular biochemistry 199 (1999), S. 103-109 
    Details
    ISSN: 1573-4919
    Keywords: antidepressive agents ; fluoxetine ; rat brain mitochondria ; oxidative phosphorylation ; H(+)transporting-ATP synthase ; ATP synthesis ; ATP hydrolysis ; 1-aniline-8-naphathalene sulfonate fluorescence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effects of fluoxetine on the oxidative phosphorylation of mitochondria isolated from rat brain and on the kinetic properties of submitochondrial particle F1F0-ATPase were evaluated. The state 3 respiration rate supported by pyruvate + malate, succinate, or ascorbate + tetramethyl-p-phenylenediamine (TMPD) was substantially decreased by fluoxetine. The IC50 for pyruvate + malate oxidation was ∼ 0.15 mM and the pattern of inhibition was the typical one of the electron-transport inhibitors, in that the drug inhibited both ADP- and carbonyl cyanide m-chlorophenylhydrazone (CCCP)-stimulated respirations and the former inhibition was not released by the uncoupler. Fluoxetine also decreased the activity of submitochondrial particle F1F0-ATPase (IC50 ∼ 0.08 mM) even though K0.5 and activity of Triton X-100 solubilized enzyme were not changed substantially. As a consequence of these effects, fluoxetine decreased the rate of ATP synthesis and depressed the phosphorylation potential of mitochondria. Incubation of mitochondria or submitochondrial particles with fluoxetine under the conditions of respiration or F1F0-ATPase assays, respectively, caused a dose-dependent enhancement of 1-anilino-8-naphthalene sulfonate (ANS) fluorescence. These results show that fluoxetine indirectly and nonspecifically affects electron transport and F1F0)-ATPase activity inhibiting oxidative phosphorylation in isolated rat brain mitochondria. They suggest, in addition, that these effects are mediated by the drug interference with the physical state of lipid bilayer of inner mitochondrial membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006912010550
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  • 4
    Electronic Resource
    Electronic Resource
    cis-Acting DNA elements involved in oocyte-specific expression of mouse sperm receptor gene mZP3 are located close to the gene's transcription start site (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 36 (1993), S. 494-499 
    Details
    ISSN: 1040-452X
    Keywords: Luciferase gene ; 153-ZP3/LUC ; ZDT ; Transgene ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: We report that cis-acting DNA elements involved in oocyte-specific expression of the mouse sperm receptor gene (mZP3) are located close to the gene's transcription start site. Mice bearing a transgene that consists of only 153 nt of mZP3 5′-flanking region fused to the firefly luciferase gene (153-ZP3/LUC) expressed the reporter gene in ovary not in a wide variety of tissues; although two of three lines carrying 153-ZP3/LUC also expressed the transgene in forebrain and hypothalamus. Within the ovaries of transgenic mice, luciferase activity was restricted to growing oocytes. However, levels of luciferase activity in these oocytes were lower than those in oocytes from mice bearing transgenes that contain a larger segment of mZP3 5′-flanking region (470-6,500 nt) fused to the firefly luciferase gene. Mice bearing a trans-gene that consists of 470 nt of mZP3 5′-flanking region and mZP3 intragenic sequences (ZDT) were also analyzed. The presence of mZP3 intragenic sequences did not result in significantly increased levels of firefly luciferase activity in oocytes of mice carrying the ZDT transgene. Overall, these results suggest that as little as 153 nt of mZP3 5′-flanking region is sufficient to target expression of the firefly luciferase gene to mouse oocytes and that the mZP3 intragenic sequences probably do not contain enhancer elements. Rather, enhancer elements are probably present between  -  153 and  -  470 nt of the mZP3 5′-flanking region. © 1993 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080360414
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of calcium deficiency on chondrocyte hypertrophy and type X collagen expression in chick embryonic sternum (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Developmental Dynamics 198 (1993), S. 284-295 
    Details
    ISSN: 1058-8388
    Keywords: Skeletogenesis ; Endochondral ossification ; Shell-less chick embryo ; Hyaline cartilage ; Extracellular matrix ; Mineralization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Maintenance of chick embryos in long-term culture without their calcareous eggshell is a useful method for studying the relationship between calcium homeostasis and cell differentiation during skeletogenesis. Previously, we have shown that in shell-less (SL) embryos, calcium deficiency induces a cartilage-like phenotype in osteogenic tissues, such as calvaria (Jacenko and Tuan [1986] Dev. Biol. 115:215). In this investigation, we have studied the relationship between cartilage calcification and hypertrophy, and the expression of type X collagen, a specific product of hypertrophic chondrocytes. For this study, the cephalic (calcifying) and caudal (permanently cartilaginous) regions of sterna from day 18 and day 20 normal (NL) and SL embryos were metabolically labeled with [14C]-proline. Analysis of the biosynthetic products revealed significant differences in type X collagen expression in the cephalic region of sternal cartilage. In NL tissues, type X collagen production increased from 13.1% of total collagen at day 18 to 43.7% at day 20. In contrast, in SL embryos, type X collagen was not detectable until day 20, when it represented only 1% of total collagen. Comparison of the NL and SL embryos with respect to their serum calcium level and sternal calcium content and histology revealed a direct relationship between low systemic calcium and limited cartilage hypertrophy, undermineralization, and decreased type X collagen production in the sternal cephalic cartilage. Supplementation of CaCO3 to SL embryos increased their serum and sternal calcium, and restored cartilage hypertrophy, mineralization, and type X collagen synthesis in the cephalic portion of the sterna. These findings confirm that a critical relationship exists between calcium homeostasis, chondrocyte hypertrophy, mineralization, and type X collagen synthesis in the cephalic region of sternal cartilage. These results further demonstrate the importance of calcium in the morphogenetic events of endochondral ossification, in particular the transition from hyaline cartilage to hypertrophic cartilage, and eventually to bone. © 1993 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001980406
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  • 6
    Electronic Resource
    Electronic Resource
    The histogenesis and cytology of the pancreatic islets in the rabbitA portion of a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in the Department of Pathology of the Graduate School of McGill University, 1950.This work was assisted by Grants-in-Aid from the National Research Council of Canada.Preliminary reports were given at the meeting of the American Association of Anatomists, Columbus, Ohio, 1953. (1955)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 96 (1955), S. 103-151 
    Details
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1000960105
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  • 7
    Electronic Resource
    Electronic Resource
    Electron microscopic observations on primary decidua formation in the ratThis investigation was supported by a Research Grant from the National Institutes of Health (HD 005690-03) and by the Medical Research Council of Canada. (1965)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 116 (1965), S. 217-235 
    Details
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Cytological changes in uterine stromal cells of the rat during induced primary decidua formation have been examined electron microscopically. Decidua forming stroma was examined at daily intervals for the five days during which the reaction reaches maximal hypertrophy and hyperplasia and was compared with pseudopregnant, non-decidual (control) endometrium. Stromal cells of control uteri resemble embryonic fibroblasts. They appear to be of two types, depending on whether they contain rough - or smooth-surfaced endoplasmic reticulum. As the decidual reaction progresses, the cells enlarge and become binucleate; cells which contain exclusively rough surface endoplasmic reticulum no longer are evident. Glycogen and fat become abundant, the former in association with smooth-surfaced membranes of the endoplasmic reticulum. Mitochondria become more numerous, smaller, and show evidence of a rearrangement in internal organization. There is a pronounced increase in a fine intracytoplasmic fibrillar component; and a spectrum of “microbodies” and lysosomes appears. At the height of the reaction, the stroma appears epithelioid. The possible functional significance of these changes is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001160111
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  • 8
    Electronic Resource
    Electronic Resource
    Extensive apoptotic death of rat colonic cells deprived of crypt habitat (1998)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 177 (1998), S. 377-386 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Apoptosis in cells of different lineages is restrained by survival signals which depend upon cell-to-cell communication. The aim of this study was to determine whether colonic cells deprived of crypt ambient are doomed to die prior to their normal chronological demise. Apoptosis was studied in rat whole colonic tissue, in isolated intact crypts, and in colonic cell populations collected from the crypt axis at different stages of proliferation and differentiation. In a number of experiments, cell harvest was performed in the presence of either a tetrapeptide (YVAD-CMK) inhibitor of interleukin-1β-converting enzyme (ICE), or tyrphostin A25, a protein tyrosine kinase inhibitor, or sodium-orthovanadate, a phosphatase inhibitor. DNA fragmentation was assessed by electrophoretic and nonisotopic-labeling procedures. The ultrastructure of colonic tissue specimens and isolated cells was examined by transmission electron microscopy. Apoptosis in whole colonic tissue and in isolated crypts was confined predominantly to cells resident in the upper crypt regions. In contrast, extensive apoptotic death was observed in isolated colonic cells, irrespective of their developmental stage and positional hierarchy within the crypt continuum at harvest time. An apoptotic gradient, however, was evident. Exposure to YVAD-CMK resulted in a marked decrease in the number of apoptotic cells. Treatment with tyrphostin A25 caused a sharp rise in the apoptotic index; conversely, vanadate significantly impeded apoptosis. Cumulatively, these results indicate that disordered intercellular communication provokes unscheduled ICE-mediated apoptosis of colonocytes, and that local signals along the crypt continuum control both the reprieve from death and the timely demise of distinct colonic cell populations. Attenuation of tyrosine phosphorylation may be a contributory event in the acquisition of the apoptotic phenotype. J. Cell. Physiol. 177:377-386, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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