Modification of glycolysis affects cell sensitivity to apoptosis induced by oxidative stress and mediated by mitochondria

Jeong, Dae Won; Kim, Tae Soo; Cho, Il Taeg; Kim, Ick Young

doi:10.1016/j.bbrc.2003.12.033

Cited by 43 publications

(47 citation statements)

References 41 publications

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“…We suggest that in this way, high glucose concentration increases the toxic effect of an oxidizing agent. This finding is in agreement with other authors' observations that high rate of substrate influx to mitochondria induces cell sensitivity to oxidant-induced apoptosis 11 . The DNA damage observed in cells at high glucose concentrations can be explained in the same way as the additive effect of glucose to tBH -increased ROS production together with insufficient restoration of glutathione 12 .…”

Section: Discussionsupporting

confidence: 94%

High Glucose Increases Susceptibility to Oxidative-Stress-Induced Apoptosis and Dna Damage in K-562 Cells

Hruda¹,

Šrámek²,

Leverve³

2010

BIOMED PAP

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glucose increases susceptibility to oxidative-stressinduced apoptosis and DNA damage in K-562 cells.. Biomedical papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia, 2010, 154 (4), pp.315-20. 315 Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2010 154(4):315-320. © J. Hruda, V. Sramek, X Methods. Glucose at 5, 11 and 30 mM concentrations was tested, as well as 5 mM glutamine and 5 mM fructose. The cells were exposed to tert-butylhydroperoxide (tBH) and apoptotic cells were evaluated by flow cytometry with FITC-Annexin V and propidium iodide. The effect of glucose concentration on DNA damage was evaluated using hydrogen peroxide and electrophoretic "DNA comets" assay at 5 mM and 30 mM glucose concentrations.Results. The exposure of cells to tBH resulted in increased number of apoptotic cells, and this effect was prevented by administration of an antioxidant -N-Acetyl cysteine. Rising concentrations of glucose added to the toxic effect of tBH; we also observed some toxic effect of fructose and no effect of glutamine. We found higher susceptibility to hydrogen peroxide induced DNA damage with 30 mM glucose concentration.Conclusion. Hyperglycemia increases the cell's susceptibility to oxidative stress and it also amplifies oxidative DNA damage. Glutamine -when used as a sole energetic substrate -showed no protective effect against oxidative stress.

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Section: Discussionsupporting

confidence: 94%

High Glucose Increases Susceptibility to Oxidative-Stress-Induced Apoptosis and Dna Damage in K-562 Cells

Hruda¹,

Šrámek²,

Leverve³

2010

BIOMED PAP

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“…Some examples are the use of the GS as a selection and amplification system and also as an optimization approach for the cellular metabolism to get rid for the need for glutamine in the culture medium (Sanders et al 1987;Bebbington et al 1992;Brown et al 1992); or the overexpression of cytosolique pyruvate carboxylase in continuous cell lines for improving the connection between glycolysis and the Krebscycle (Irani et al 1999: BHK21;Elias et al 2003: HEK293); or the overexpression of anti-sense LDH-A and of cytoplasmic glycerol-3-phosphate dehydrogenase in CHO cells for increasing the oxidative phosphorylation, for decreasing cellular respiration and thus reducing sensitivity to reactive oxygen species and overall, reducing apoptosis (Jeong et al 2004). Cellular behaviour against environmental stress conditions is often characterized by an induction of apoptosis, thus leading to a precious loss of viable biomass and the stopping of a productive culture.…”

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confidence: 99%

Introduction to animal cell culture technology—past, present and future

Merten

2006

Cytotechnology

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“…Previous studies have also shown that ATP content can be maintained or even enhanced after treatment with dissipaters of mitochondrial membrane (15,17,18) but not after inhibitors of glycolysis (16). Noda et al (27) have shown that inhibition of oxidative phosphorylation results in a buildup of reduced nicotinamide adenine dinucleotide in the mitochondria and retrogressively into the cytoplasm, resulting in an enhanced rate of lactate formation (which requires reduced nicotinamide adenine dinucleotide).…”

Section: Discussionmentioning

confidence: 95%

“…Loss of mitochondrial membrane potential is associated with changes in the energy status of cells (15)(16)(17)(18) and so is likely to influence the incorporation of 18 F-FDG. The mitochondrial membrane can be depolarized by treating cells with the selective K 1 ion channel-opening agent valinomycin.…”

mentioning

confidence: 99%

Treatment of Breast Tumor Cells In Vitro with the Mitochondrial Membrane Potential Dissipater Valinomycin Increases 18F-FDG Incorporation

Smith

Blaylock²

2007

Journal of Nuclear Medicine

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Mitochondrial membrane potential is essential for adenosine triphosphate (ATP) synthesis by oxidative phosphorylation, and its abolition is an early event during apoptosis, a type of cell death commonly exhibited by tumor cells responding to treatment. Dissipation of mitochondrial membrane potential can be specifically induced using the K 1 ion channel-opening agent valinomycin and has been used in this study to determine how the loss of mitochondrial membrane potential could influence 18 F-FDG incorporation. Methods: MCF-7 cells were treated with valinomycin for 30 min, inducing loss of mitochondrial membrane potential as determined using flow cytometry with the JC-1 probe. 18 F-FDG incorporation, the initial rate of O-methyl-D-glucose incorporation (a measure of glucose transport), hexokinase activity and subcellular distribution, ATP content using bioluminescence, and lactate production were determined on control and valinomycin-treated cells. Results: A 30-min treatment of MCF-7 cells with 1 mmol of valinomycin per liter resulted in absence of red fluorescence from JC-1, indicative of dissipation of mitochondrial membrane potential. 18 F-FDG incorporation was significantly increased by 30 min of treatment with valinomycin and was still apparent after 3.5 h of incubation. Hexokinase activity and subcellular distribution were not significantly different between control cells and cells treated for 30 min with valinomycin. Glucose transport was moderately though significantly increased, and lactate production was also increased. Conclusion: Loss of mitochondrial membrane potential is associated with increased 18 F-FDG incorporation, glucose transport, and lactate production.

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Modification of glycolysis affects cell sensitivity to apoptosis induced by oxidative stress and mediated by mitochondria

Cited by 43 publications

References 41 publications

High Glucose Increases Susceptibility to Oxidative-Stress-Induced Apoptosis and Dna Damage in K-562 Cells

High Glucose Increases Susceptibility to Oxidative-Stress-Induced Apoptosis and Dna Damage in K-562 Cells

Introduction to animal cell culture technology—past, present and future

Treatment of Breast Tumor Cells In Vitro with the Mitochondrial Membrane Potential Dissipater Valinomycin Increases 18F-FDG Incorporation

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