Reference : Reversibility of thiamine deficiency-induced partial necrosis and mitochondrial uncou...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/8574
Reversibility of thiamine deficiency-induced partial necrosis and mitochondrial uncoupling by addition of thiamine to neuroblastoma cell suspensions.
English
Bettendorff, Lucien mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biochimie et physiologie humaine et pathologique >]
Goessens, Guy mailto [Université de Liège - ULg > Services généraux (Faculté des sciences) > Relations académiques et scientifiques (Sciences) >]
Sluse, Francis mailto [Université de Liège - ULg > Département des sciences de la vie > Bioénergétique et physiologie cellulaire >]
1997
Molecular and Cellular Biochemistry
Kluwer Academic Publishers
174
1-2
121-4
Yes (verified by ORBi)
International
0300-8177
The Hague
The Netherlands
[en] Electron Transport ; Humans ; Mitochondria/metabolism/pathology ; Necrosis ; Neuroblastoma/metabolism/pathology/ultrastructure ; Oxygen Consumption ; Thiamine Deficiency/metabolism/pathology ; Tumor Cells, Cultured
[en] Culture of neuroblastoma cells in the presence of low thiamine concentration (16 nM) and of the transport inhibitor amprolium leads to the appearance of signs of necrosis: the chromatin condenses, the oxygen consumption decreases and is uncoupled, the mitochondrial cristae are disorganized, the thiamine diphosphate-dependent dehydrogenase activities are impaired. When 10 microM thiamine are added to these cells, the basal respiration increases, the coupled respiration is restored and mitochondrial morphology is recovered within 1 h. Addition of succinate, which is oxidized via a thiamine diphosphate-independent dehydrogenase, to digitonin-permeabilized cells immediately restores a coupled respiration. Our results suggest that the slowing of the citric acid cycle is the cause of the biochemical lesion induced by severe thiamine deficiency and that part of the mitochondria remain functional.
http://hdl.handle.net/2268/8574
also: http://hdl.handle.net/2268/4655 ; http://hdl.handle.net/2268/32866

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