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An Optimized Protocol to Analyze Glycolysis and Mitochondrial Respiration in Lymphocytes
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An Optimized Protocol to Analyze Glycolysis and Mitochondrial Respiration in Lymphocytes

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

Dae-won Jeong1, Tae-Soo Kim, Il Taeg Cho

  • 1BK21 Human Life Sciences, Seoul National University, Seoul, Republic of Korea.

Biochemical and Biophysical Research Communications
|January 7, 2004
PubMed

Insights

Altering the glycolytic pathway impacts cell damage from oxidative stress. Increased mitochondrial respiration enhances resistance to oxidative death, while decreased respiration increases sensitivity.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Oxidative Stress Research

Background:

  • Oxidative stress can induce cell damage and apoptosis.
  • The glycolytic pathway plays a role in cellular metabolism and response to stress.
  • Mitochondrial function is critical in determining cell fate under stress.

Purpose of the Study:

  • To investigate how altering the glycolytic pathway affects oxidative stress-induced cell damage.
  • To determine the role of mitochondrial respiration in cell sensitivity to oxidants.

Main Methods:

  • Utilized dihydrofolate reductase-deficient Chinese hamster ovary (CHO) cells with modified glycolytic pathways (overexpressing cytosolic glycerol-3-phosphate dehydrogenase or depleted of lactate dehydrogenase A subunit).
  • Measured intracellular ATP, cellular O(2) consumption, mitochondrial membrane potential (DeltaPsi(m)), and reactive oxygen species generation.
  • Assessed cell death via apoptosis markers (subdiploid DNA content, DeltaPsi(m) collapse, cytochrome c release) after exposure to tert-butyl hydroperoxide.

Main Results:

  • Cells with increased oxidative phosphorylation (CHO/anti-LDH) showed higher resistance to oxidant-induced death compared to parental CHO cells.
  • Cells with decreased oxidative phosphorylation (CHO/cGPDH) were more sensitive to oxidant-induced death.
  • Exogenous pyruvate increased the sensitivity of CHO/cGPDH cells to oxidant-induced death.
  • Apoptosis was confirmed as the mechanism of cell death, indicated by DNA fragmentation, mitochondrial dysfunction, and cytochrome c release.

Conclusions:

  • The glycolytic pathway significantly influences cellular sensitivity to oxidative stress.
  • Mitochondrial substrate influx is a key factor in determining susceptibility to oxidant-induced apoptosis.
  • Targeting mitochondrial respiration could be a strategy to modulate cell death in response to oxidative stress.

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