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  • 1
    Electronic Resource
    Electronic Resource
    Induction of apoptotic cell death in rat thymus and spleen after a bolus injection of methamphetamine (1996)
    Springer
    International journal of legal medicine 109 (1996), S. 23-28 
    Details
    ISSN: 1437-1596
    Keywords: Apoptosis ; Methamphetamine ; Lymphocytes ; Thymus ; Spleen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Law
    Notes: Abstract We examined whether methamphetamine (MAP) induced apoptotic cell death in vivo. Male Wistar rats were injected intraperitoneally with 25 mg MAP/Kg body weight and were sacrificed at 4, 8 and 24 h. As early as 4 h after a single dose of MAP, DNA ladder bands representing DNA fragmentation into multiples of the internucleosomal DNA length of about 180 by were observed by gel electrophoresis in thymic and splenic DNA. DNA from control rats injected with 1 ml physiological saline/Kg body weight showed no ladder band patterns. The proportion of fragmented DNA from the thymus increased in a time-dependent manner up to 8 h and faint ladder band patterns were observed at 24 h, indicating that cell death via apoptosis occurred at an early stage and then apoptotic bodies were scavenged. DNA fragmentation in the thymus and spleen induced with MAP was also confirmed by the terminal deoxynucleotidyl transferase-mediated dUTPbiotin nick end labeling (TUNEL) method in situ. In control thymus samples, stained cells were numerous in the cortex but sparse in the medulla. At the boundary area between the cortex and medulla, stained cells were seen as a layer. In the MAP-treated rats, stained cells were increased and dispersed equally in the cortex and medulla. In control spleen samples, stained cells were numerous in all areas excluding the germinal centers. Cells at the germinal centers were stained intensively in MAP-treated rat spleen. Light microscopical analyses allowed us to identify lymphocytes during the course of apoptotic cell death. Electron microscopic studies showed morphological landmarks for the process of cellular apoptosis in both organs e.g. lymphocytes with chromatin condensed into crescents at the periphery of the nuclei and apoptotic bodies. These results indicate that MAP induced cell death of the thymic and splenic lymphocytes via apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01369597
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Senescence marker protein-30 (SMP30) enhances the calcium efflux from renal tubular epithelial cells (1999)
    Springer
    Clinical and experimental nephrology 3 (1999), S. 261-267 
    Details
    ISSN: 1437-7799
    Keywords: Key words SMP30 ; Calcium efflux ; Tubular epithelia ; Calcium pump ; Calmodulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. Senescence marker protein-30 (SMP30), a calcium binding protein, is preferentially expressed in the renal proximal tubules and hepatocytes and is presumed to play a role in Ca2+ homeostasis. Methods. To explore its physiological functions in the tubular cells, we investigated the effect of SMP30 on Ca2+ efflux via the ATP-dependent plasma membrane calcium pump. LLC-PK1 cells were stably transfected with a cDNA encoding SMP30, and the established transfectants were subjected to ATP responses. Results. Overexpression of SMP30 significantly increased Ca2+ efflux under both basal and ATP-stimulated conditions. Inhibition of calmodulin by trifluoperazine abrogated the enhanced Ca2+ efflux, suggesting that SMP30 activated the calmodulin-dependent Ca2+ pump. It is known that Ca2+ superfluous influx induces cellular injury. Compared with mock-transfected cells, LLC-PK1 cells expressing SMP30 showed resistance to cellular death triggered by Ca2+ superfluous influx. Conclusion. These results suggest the possibility that, in renal tubular cells, endogenous SMP30 participates in Ca2+ efflux via activating the calmodulin-dependent Ca2+ pump and thereby confers resistance of the cells against injury caused by high intracellular Ca2+ concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101570050045
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    Paper (German National Licenses)
    Fulltext
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