Effect and function of biological buffer PEP

Details:

Phosphoenolpyruvate (PEP) is a glycolytic metabolite with high-energy phosphate group. PEP (0.1-10 mm) significantly attenuated the decrease of cell viability induced by hydrogen peroxide (H (2) O (2)) in HeLa cells in a dose-dependent manner. PEP also inhibited the decrease of calcein acetylmethoxy stained cells and the increase of propidium iodide stained cells induced by H (2) O (2). The increase of intracellular reactive oxygen species stimulated by hep (2) O (2) decreased significantly.

PEP is a functional carbohydrate metabolite with cytoprotective and antioxidant activities, and may be used as a therapeutic agent for diseases involving oxidative stress. However, no effect was shown at low doses (0.1, 1 mm). PEP (0.1-10 mm) also reduced cell damage, but did not reduce the decrease of intracellular ATP content induced by glycolysis inhibitor 2-deoxy-D-glucose.

PEP can also reduce the increase of aminotransferase and lactate dehydrogenase leakage during organ preservation, histological changes and changes in oxidative stress parameters (measured by thiobarbituric acid reactive substances and glutathione content) caused by liver preservation for 72 hours. Its effect is comparable to that of the University of Wisconsin solution, a gold standard organ preservation agent. PEP treatment could reduce the decrease of ATP content in liver during cold storage. PEP prevented the cell damage of HepG2 cells and increased the content of intracellular reactive oxygen species. In addition, PEP scavenged hydroxyl radical, but had no effect on superoxide anion, which was evaluated by electron paramagnetic resonance spin trapping technique.

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