2003
DOI: 10.1016/s0167-4889(03)00105-8
|View full text |Cite
|
Sign up to set email alerts
|

Changes of mitochondrial respiration, mitochondrial content and cell size after induction of apoptosis in leukemia cells

Abstract: 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,… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

7
64
0
1

Year Published

2005
2005
2018
2018

Publication Types

Select...
8
1

Relationship

1
8

Authors

Journals

citations
Cited by 111 publications
(72 citation statements)
references
References 38 publications
7
64
0
1
Order By: Relevance
“…Previous investigations have shown that dexamethasone (Dex), a synthetic glucocorticoid, reduces the survival and induces the apoptosis of thymocytes, leukemia and insulin-secreting cells (5)(6)(7)(8)(9), and the effect is mediated through the release of mitochondrial cytochrome c (5,6), the activation of caspases and generation of reactive oxygen species (8), the inhibition of nuclear factor-ÎşB (9,10), and/or the inhibition of phosphorylation of insulin receptor substrate-2 and protein kinase B (PKB) (11). A large body of evidence also demonstrates that Dex treatment leads to alteration of the expression and/or activities of many intracellular signaling proteins (12)(13)(14), including mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) and the family of MAPKs, which are involved in gene expression, cell survival and/or apoptosis.…”
Section: Introductionmentioning
confidence: 99%
“…Previous investigations have shown that dexamethasone (Dex), a synthetic glucocorticoid, reduces the survival and induces the apoptosis of thymocytes, leukemia and insulin-secreting cells (5)(6)(7)(8)(9), and the effect is mediated through the release of mitochondrial cytochrome c (5,6), the activation of caspases and generation of reactive oxygen species (8), the inhibition of nuclear factor-ÎşB (9,10), and/or the inhibition of phosphorylation of insulin receptor substrate-2 and protein kinase B (PKB) (11). A large body of evidence also demonstrates that Dex treatment leads to alteration of the expression and/or activities of many intracellular signaling proteins (12)(13)(14), including mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) and the family of MAPKs, which are involved in gene expression, cell survival and/or apoptosis.…”
Section: Introductionmentioning
confidence: 99%
“…To reduce the impact of this factor, some authors propose to express the tissue respiration data per citrate synthase activity (Renner et al, 2003).…”
Section: Discussionmentioning
confidence: 99%
“…The cytotoxicity induced by EFTB was determined by the quantitative estimation of cytoplasmic lactate dehydrogenase (LDH) leaked into the culture medium by the method of Renner et al, 2003(Renner et al, 2003. Briefly, after the exposure of cell lines to the different concentrations of EFTB, the culture medium was aspirated and centrifuged at 4000 rpm for 10 min to get cell free supernatant.…”
Section: Neutral Red Cell Viability Assay:-mentioning
confidence: 99%