Document Detail

A decrease in intracellular glutathione concentration precedes the onset of apoptosis in murine thymocytes.
MedLine Citation:
PMID:  8549589     Owner:  NLM     Status:  MEDLINE    
Free radical damage has been implicated in the induction of apoptosis in some cells. We investigated whether the status of a cell's oxidant defence system is involved in the signalling pathways triggering apoptosis. We used three unrelated agents, dexamethasone, thapsigargin and gliotoxin to induce apoptosis in thymocytes from 10-day-old BALB/c mice. With all stimuli there was a correlation between the percentage of cells undergoing apoptosis (as measured with propidium iodide DNA staining) and the percentage of cells with lowered [GSH]i. Treatment with either 1 mM reduced glutathione or 10 nM thapsigargin inhibited dexamethasone-induced apoptosis in thymocytes at 6 h, as well as the rise in the percentage of cells with lowered [GSH]i that normally accompanied the onset of apoptosis. Furthermore, following treatment of thymocytes with oxidized glutathione, a normal product of the action of the cell's oxidant defence system, high levels of apoptosis were observed. This suggested that the onset of apoptosis was not simply the result of a loss of GSH from the cytosol. From our evidence we suggest that a decrease in [GSH]i, or an increase in [GSSG]i or perhaps a change in the ratio of [GSH]i to [GSSG]i constitutes a trigger for apoptosis.
J P Beaver; P Waring
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  European journal of cell biology     Volume:  68     ISSN:  0171-9335     ISO Abbreviation:  Eur. J. Cell Biol.     Publication Date:  1995 Sep 
Date Detail:
Created Date:  1996-02-22     Completed Date:  1996-02-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906240     Medline TA:  Eur J Cell Biol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  47-54     Citation Subset:  IM    
Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra/Australia.
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MeSH Terms
Apoptosis / drug effects,  physiology*
Calcium-Transporting ATPases / antagonists & inhibitors
Dexamethasone / pharmacology
Enzyme Inhibitors / pharmacology
Gliotoxin / pharmacology
Glucocorticoids / pharmacology
Glutathione / analogs & derivatives,  metabolism*
Glutathione Disulfide
Terpenes / pharmacology
Thymus Gland / cytology,  drug effects,  metabolism*
Time Factors
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Glucocorticoids; 0/Terpenes; 27025-41-8/Glutathione Disulfide; 50-02-2/Dexamethasone; 67-99-2/Gliotoxin; 67526-95-8/Thapsigargin; 70-18-8/Glutathione; EC ATPases

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