Renner 2002 Mol Biol Rep

From Bioblast
Revision as of 14:09, 27 December 2021 by Gnaiger Erich (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision β†’ (diff)
Publications in the MiPMap
Renner K, Kofler R, Gnaiger E (2002) Mitochondrial function in glucocorticoid triggered T-ALL cells with transgenic Bcl-2 expression. Mol Biol Rep 29:97-101.

Β» PMID: 12241083

Renner K, Kofler R, Gnaiger Erich (2002) Mol Biol Rep

Abstract: Independent of apoptosis, dexamethasone induced and a decrease of respiration and citrate synthase activity per cell in cells with and without transgenic Bcl-2 expression. The reduction of respiration, however, was slightly, but statistically more pronounced in apoptotic cells compared to non-apoptotic Bcl-2 over-expressing cells. A slight cytochrome c release was detected in apoptotic cells only. Importantly, the stimulatory effect of FCCP was maintained, indicating that oxidative phosphorylation remained coupled in active mitochondria. Coupled and uncoupled respiration were reduced to almost identical degrees as the activities of the marker enzymes citrate synthase (matrix) and cytochrome c oxidase (respiratory chain). Therefore, the reduction of cellular respiration was mainly caused by a decrease in mitochondrial content per cell. The functional integrity of mitochondria was preserved, apart from the slight degree of cytochrome c release, either through a pore formed by the oligomerisation of BAK in coupled mitochondria or by permeability transition of a small fraction of injured mitochondria.

β€’ O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros, DE Regensburg Renner-Sattler K

Cited by

Labels: MiParea: Respiration, Genetic knockout;overexpression, Pharmacology;toxicology  Pathology: Cancer  Stress:Cell death  Organism: Human  Tissue;cell: Blood cells  Preparation: Intact cells 

Coupling state: ROUTINE 

HRR: Oxygraph-2k 

Cookies help us deliver our services. By using our services, you agree to our use of cookies.