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  1. 1
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    Nature Publishing Group (NPG)
    Published 2015
    Staff View
    Publication Date:
    2015-01-22
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Adolescent ; Adult ; Aged ; Aged, 80 and over ; Aging/genetics ; Apoptosis/genetics ; Brain/*anatomy & histology ; Caudate Nucleus/anatomy & histology ; Child ; Female ; Gene Expression Regulation, Developmental/genetics ; Genetic Loci/genetics ; Genetic Variation/*genetics ; *Genome-Wide Association Study ; Hippocampus/anatomy & histology ; Humans ; Magnetic Resonance Imaging ; Male ; Membrane Proteins/genetics ; Middle Aged ; Organ Size/genetics ; Putamen/anatomy & histology ; Sex Characteristics ; Skull/anatomy & histology ; Young Adult
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Cookson, M. R. ; Slamon, N. D. ; Pentreath, V. W.
    Springer
    Published 1998
    Staff View
    ISSN:
    1432-0738
    Keywords:
    Key words C6 cells ; Astrocytes ; Triethyltin ; Trimethyltin ; Glutathione
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract It has been demonstrated that exposure to mercury or cadmium compounds causes alterations in the glutathione system in a model glial cell line, C6. Here we report that two organic tin compounds, triethyltin (TET) and trimethyltin (TMT), are also toxic to these cells with EC50 values for cell death of c. 0.02 μM and 0.8 μM respectively. Exposure for 24 h to either of these compounds at sub-toxic concentrations caused increases in the amount of reduced glutathione (GSH) per cell. Increases in glutathione-S-transferase enzyme activity were also demonstrated after TET or TMT exposure. This suggests that glutathione increases occur in glial cells after toxic insults below that required to cause cell death, possibly acting as a protective mechanism. To test whether GSH plays a role in organotin-induced cell death we manipulated GSH in the culture media or via intracellular GSH and looked at the effects on sensitivity to TET or TMT toxicity. Adding GSH to the culture media did not protect the cells. Depletion of intracellular GSH with buthionine-[S,R] sulphoximine did not alter cytotoxicity of TET or TMT. However, pre-treatment with (−)-2-oxo-4-thiazolidine carboxylic acid (OTC), which increases intracellular GSH levels, protected the cells against both compounds. The EC50 for TMT was increased from 0.77 to 1.8 μM, a 2.3-fold shift, whereas the EC50 for TET was increased 〉20-fold, from 0.022 to 0.47 μM. One interpretation of these results is that GSH protects cells against the toxicity of organic tin compounds without reacting directly with them to any significant extent. Under conditions where GSH is depleted, additional protective mechanisms may be active.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s002040050488

    Articles: DFG German National Licenses
  3. 3
    Alafiatayo, R. A. ; Cookson, M. R. ; Pentreath, V. W.
    Springer
    Published 1994
    Staff View
    ISSN:
    1432-1955
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Biology
    Medicine
    Notes:
    Abstract A study was made to characterize the effects of livingTrypanosoma brucei brucei and its products on prostaglandin D2 (PGD2) and PGE2 production by fibroblasts and astrocytes. Cultured fibroblasts were prepared fromMicrotus agrestis embryos and astrocyte cultures were prepared from neonatal rats. The cultures were maintained in low-endotoxin or defined media (i.e. endotoxin-free). The PG production was compared with and studied in combination with a defined lipopolysaccharide (LPS) fromEscherichia coli. LivingT. b. brucei were without effect on PG production. Preparations ofT. b. brucei prepared by freeze-thawing and sonication produced dose- and time-dependent increases in PGD2 and PGE2 synthesis by both cell types. LPS caused a similar pattern of increases. The combination of parasite products with LPS caused synergistic production to levels higher than the maximal production by each mitogen alone. The findings have important implications for several pathological features that accompany trypanosomiasis.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00932678

    Articles: DFG German National Licenses