Reference : Thiamine Deficiency--Induced Partial Necrosis and Mitochondrial Uncoupling in Neuroblast...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/5710
Thiamine Deficiency--Induced Partial Necrosis and Mitochondrial Uncoupling in Neuroblastoma Cells Are Rapidly Reversed by Addition of Thiamine
English
Bettendorff, Lucien mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biochimie et physiologie humaine et pathologique >]
Sluse, Francis mailto [Université de Liège - ULg > Département des sciences de la vie > Bioénergétique et physiologie cellulaire >]
Goessens, Guy mailto [Université de Liège - ULg > Services généraux (Faculté des sciences) > Relations académiques et scientifiques (Sciences) >]
Wins, Pierre [> > > >]
Grisar, Thierry mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biochimie et physiologie humaine et pathologique]
1995
Journal of Neurochemistry
65
5
2178-2184
Yes (verified by ORBi)
International
0022-3042
[en] Thiamine defiency ; necrosis ; Uncoupling ; Mitochondria ; Neuroblastoma cells
[en] Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled, and their cristae are disorganized. Glutamate formed from glutamine is no longer oxidized and accumulates, suggesting that the thiamine diphosphate-dependent alpha-ketoglutarate dehydrogenase activity is impaired. When thiamine (10 microM) is added to the cells, the O2 consumption increases, respiratory control is restored, and normal cell and mitochondrial morphology is recovered within 1 h. Succinate, which is oxidized via the thiamine diphosphate-independent succinate dehydrogenase, is also able to restore a normal O2 consumption (with respiratory control) in digitonin-permeabilized thiamine-deficient cells. Our results therefore suggest that the slowing of the citric acid cycle is the main cause of the biochemical lesion induced by thiamine deficiency as observed in Wernicke's encephalopathy.
http://hdl.handle.net/2268/5710
also: http://hdl.handle.net/2268/4612

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