Renner 2003 Biochim Biophys Acta

From Bioblast
Jump to navigation Jump to search
Publications in the MiPMap
Renner K, Amberger A, Konwalinka G, Gnaiger E (2003) Changes of mitochondrial respiration, mitochondrial content and cell size after induction of apoptosis in leukemia cells. Biochim Biophys Acta 1642:115-23.

» PMID: 12972300

Renner-Sattler Kathrin, Amberger A, Konwalinka G, Gnaiger Erich (2003) Biochim Biophys Acta


Renner 2003 BBA-mt-density.jpg

Mitochondrial damage with release of cytochrome c is implicated in cell death signalling pathways. To examine mitochondrial function in apoptotic cells, we applied high-resolution respirometry to human leukemia cells arrested in the G1- and S-phase by exposure to the glucocorticoid dexamethasone and nucleotide analogue gemcitabine. At 30 % apoptosis, opposite effects were observed on respiratory capacity (71 % and 131 % of controls, respectively). These changes correlated with alterations in cell size, cytosolic, and mitochondrial marker enzymes. Mitochondrial ATP production and membrane potential were maintained in all treatments, as deduced from high respiratory uncoupling control ratios. Bcl-2 over-expression did not prevent apoptosis after gemcitabine-treatment, but protected dexamethasone-treated cells from apoptosis, without fully preventing the decline of respiration and cell size.

These results, therefore, provide conclusive evidence that alterations in respiratory capacity and enzyme activities per cell are mainly caused by opposite changes in cell size, occurring upon cell cycle arrest triggered by dexamethasone and gemcitabine in the early phase of apoptosis.

Keywords: Apoptosis, Dexamethasone, Gemcitabine, Mitochondrial respiratory control, Cell cycle

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

Cited by

Gnaiger 2020 BEC MitoPathways

Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2:112 pp. doi:10.26124/bec:2020-0002
Gnaiger Erich et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1.

Gnaiger E et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1. doi:10.26124/bec:2020-0001.v1.

Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression, Pharmacology;toxicology  Pathology: Cancer  Stress:Cell death  Organism: Human  Tissue;cell: Blood cells  Preparation: Permeabilized cells, Enzyme, Oxidase;biochemical oxidation, Intact cells 

Regulation: Coupling efficiency;uncoupling, Cyt c  Coupling state: ROUTINE, ET 

HRR: Oxygraph-2k 

Leukemia, Mitochondrial marker, BEC 2020.1, BEC 2020.2