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Using the experimental platform provided by Lanzhou Heavy Ion Accelerator National Laboratory and the Chinese Academy of Sciences Heavy Ion Beam Radiation Biomedical Key Laboratory, researchers from the Radiation Medicine Department of the Institute of Modern Physics of the Chinese Academy of Sciences have made new progress in studying exogenous positive charges to replace protons and constructing mitochondrial prosthetic membrane induced cell autophagy.
results were published in Autophagy, 2017, 13 (4): 1-9 (DOI:10.1080/15548627.2017.1280219).
nucleus cells use the membrane breathing chain in mitochondrials to oxidize NADH and FADH2, which are accompanied by protons and pumped into the mitochondrial membrane gap.
the production of protons causes the membrane gap to accumulate a large amount of positive charge, forming a potential difference across both sides of the mitochondrial membrane (Mitochondrial Membrane Potential, MMP), or mitochondrial membrane potential for short.
under the effect of this potential energy, protons flow back from membrane clearance to mitochondrial substates to drive phosphate oxide reactions and synthesize large amounts of ATP.
of these cells comes from mitochondrials, and membrane gap proton gradients are the driving force behind energy synthesis.
Researchers found that MitoQ, a liposuction cation reagent, was able to adapt to poor potential and target the insertion of mitochondrial membranes, and that the positive charge carried by its tripyl phosphorus cation cluster (TPP plus) was heavily mixed into membrane gap protons, causing MMP to rise rapidly.
in order to maintain MMP stability, cell compensation inhibits the activity of respiratory chain complexes I., III., IV. and reduces the pumping rate of protons.
With the decrease of proton supplementation in membrane clearance and the increase of TPP-richness, the final exogenous positive charge replaces protons and establishes mitochondrial prosthetic membrane potential (Pseudo-MMP, PMMP) maintained by exogenous positive charge (Figure 1).
the production of mitochondrial prosthetic membrane potential causes the reduction of the flow back of protons through ATP, the decrease of oxygen consumption of cells' breathing, and abnormal energy metabolism, which causes cell hunger.
ATP decreases, AMP increases, activates an important "energy sensor" in the cell - AMPK (AMP-dependent protein kinase), and the activated AMPK inhibits phosphorylation of mTOR (mammalian repamycin target protein) and induces cell autophagy (Figure 2).
This study first discovered mitochondrial prosthesis potential in ethnocytes and pioneered the name "Pseudo-Mitochondrial Membrane Potential";
of mitochondrial prosthesis induced cell autophagy provides a new idea for the study of precision radiation protection of normal tissue implicated in tumor radiation therapy.
the study was supported by the National Natural Science Foundation of China, the Joint Fund for Great Scientific Installations of the Chinese Academy of Sciences, the National Natural Science Foundation of China and the Western Talent Project of the Chinese Academy of Sciences.
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