Pyruvate protects mitochondria from oxidative stress in human neuroblastoma SK-N-SH cells

Xiaofei Wang, Evelyn Perez, Ran Liu, Liang Jun Yan, Robert T. Mallet, Shao Hua Yang

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136 Scopus citations


Oxidative stress is implicated in neurodegenerative diseases including stroke, Alzheimer's disease and Parkinson's disease, and has been extensively studied as a potential target for therapeutic intervention. Pyruvate, a natural metabolic intermediate and energy substrate, exerts antioxidant effects in brain and other tissues susceptible to oxidative stress. We tested the protective effects of pyruvate on hydrogen peroxide (H2O2) toxicity in human neuroblastoma SK-N-SH cells and the mechanisms underlying its protection. Hydrogen peroxide insult resulted in 85% cell death, but co-treatment with pyruvate dose-dependently attenuated cell death. At concentrations of ≥ 1 mM, pyruvate totally blocked the cytotoxic effects of H2O2. Pyruvate exerted its protective effects even when its administration was delayed up to 2 h after H2O2 insult. As a scavenger of reactive oxygen species (ROS), pyruvate dose-dependently attenuated H2O2-induced ROS formation, assessed from 2,7-dichlorofluorescein diacetate fluorescence. Furthermore, pyruvate suppressed superoxide production by submitochondrial particles, and attenuated oxidative stress-induced collapse of the mitochondrial membrane potential. Collectively, these results suggest that pyruvate protects neuronal cells through its antioxidant actions on mitochondria.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalBrain Research
Issue number1
StatePublished - 9 Feb 2007


  • Hydrogen peroxide
  • Mitochondria
  • Neuroprotection
  • Oxidative stress
  • Pyruvate
  • Superoxide


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