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Articles in PresS, published online ahead of print May 15, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00013.2002
Submitted on January 14, 2002
Accepted on May 9, 2002
1 Unite de recherche hepatologique, Centre de recherche du CHUM-Hopital Saint-Luc, Montreal, Quebec, Canada; Departement de Pharmacologie, Universite de Montreal, Montreal, Quebec, Canada
2 Unite de recherche hepatologique, Centre de recherche du CHUM-Hopital Saint-Luc, Montreal, Quebec, Canada
3 Departement de Chimie-Biochimie, Universite du Quebec a Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: Marc.Bilodeau{at}umontreal.ca.
The involvement of reduction/oxidation (redox) state in cell sensitivity to apoptosis has been suggested by several studies in which induction of apoptosis was shown to require oxidative stress or GSH extrusion. On the other hand, biochemical studies of caspases revealed that their activation necessitates a reduced cysteine in their active site : This is ensured by maintaining intact intracellular glutathione status during apoptotic induction as reported by in vivo studies. Therefore, we investigated the relationship between intracellular glutathione levels and the sensitivity of mouse hepatocytes in culture to Fas-induced apoptosis as well as potential mechanisms responsible for this sensitivity. We found that total and reduced glutathione levels are decreased by half following cell isolation procedure and further decline by 25% during cell culture for 2h in normal Williams'E medium. Cell culture in medium supplemented with cysteine and methionine maintains glutathione at a level similar to that measured just after cell isolation. Results show that the capacity of Fas to activate caspase-8 and to induce apoptosis requires important intracellular glutathione levels and high GSH/GSx ratio. In conclusion, the present study shows that intracellular glutathione plays an important role in maintaining the apoptotic machinery functional and thus capable of transmitting the apoptotic signal.
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